Статті в журналах: "T cells responses"

1

Tadokoro, Carlos E., Guy Shakhar, Shiqian Shen, Yi Ding, Andreia C. Lino, Antonio Maraver, Juan J. Lafaille, and Michael L. Dustin. "Regulatory T cells inhibit stable contacts between CD4+ T cells and dendritic cells in vivo." Journal of Experimental Medicine 203, no. 3 (March 13, 2006): 505–11. http://dx.doi.org/10.1084/jem.20050783.

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Regulatory T (T reg) cells exert powerful down-modulatory effects on immune responses, but it is not known how they act in vivo. Using intravital two-photon laser scanning microscopy we determined that, in the absence of T reg cells, the locomotion of autoantigen-specific T cells inside lymph nodes is decreased, and the contacts between T cells and antigen-loaded dendritic cells (DCs) are of longer duration. Thus, T reg cells can exert an early effect on immune responses by attenuating the establishment of stable contacts during priming of naive T cells by DCs.

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2

Krawczyk, Connie M., Hao Shen, and Edward J. Pearce. "Memory CD4 T Cells Enhance Primary CD8 T-Cell Responses." Infection and Immunity 75, no. 7 (April 16, 2007): 3556–60. http://dx.doi.org/10.1128/iai.00086-07.

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ABSTRACT CD4 T-cell help is required for optimal memory CD8 T-cell responses. We have found that engaging preexisiting CD4 Th1, but not Th2, memory cells at the time of CD8 T-cell priming results in increased CD8 effector responses to both bacterial and viral pathogens. The enhanced responses are characterized by increased numbers of cytokine-producing, antigen-specific cells. These findings suggest that engaging endogenous memory Th1 cells may increase cellular responses in an immunotherapy or vaccination setting.

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Jiang, Xiaodong, Rachael Clark, Luzheng Liu, Julien Seneschal, Rahul Purwar, Tian Tian, Robert Fuhlbrigge, and Thomas Kupper. "CD4+ T cells regulate skin resident memory CD8+ T cells (TRM) (49.8)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 49.8. http://dx.doi.org/10.4049/jimmunol.188.supp.49.8.

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Abstract The requirement of CD4+ T cell help for CD8+ T cell responses has been extensively explored in secondary lymphoid organs using systemic infection models. Whether such help also exists in peripheral tissues like the skin is unknown. We recently reported that skin resident memory CD8+ T cells (TRM) are non-recirculating and are superior to central memory CD8+ T cells (TCM) in protecting against re-infection. Interestingly, we also found that the acute CD8+ T cell migration into infected skin does not require CD4+ T cell help. Further study showed that the acute protection response of CD8+ T cells in the skin was equivalent in wild type and CD4-deficient mice. We next asked the role of CD4+ T cells in CD8+ TRM protective responses in the skin. To our surprise, the absence of CD4+ T cells did not impair the survival of CD8+ TRM in the skin. However, the recall response of CD8+ TRM in previously infected skin was significantly compromised in CD4-/- mice. The viral load assay further showed that the recall response of CD8+ TRM was significantly compromised when memory CD4+ T cells in the skin were depleted, suggesting that signals from memory CD4+ T cells in the skin are delivered to CD8+ TRM locally. Taken together, these data imply that while CD4+ T cells are not required both for acute CD8+ T cell response and maintenance CD8+ TRM in the skin, they do play an important role in regulating recall responses of CD8+ TRM.

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Chauhan, Priyanka, Shuxian Hu, Wen S. Sheng, and James R. Lokensgard. "Regulatory T-Cells Suppress Cytotoxic T Lymphocyte Responses against Microglia." Cells 11, no. 18 (September 9, 2022): 2826. http://dx.doi.org/10.3390/cells11182826.

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Regulatory T-cells (Tregs) play pivotal roles during infection, cancer, and autoimmunity. In our previous study, we demonstrated a role for the PD-1:PD-L1 pathway in controlling cytolytic responses of CD8+ T lymphocytes against microglial cells presenting viral peptides. In this study, we investigated the role of Tregs in suppressing CD8+ T-cell-mediated cytotoxicity against primary microglial cells. Using in vitro cytotoxicity assays and flow cytometry, we demonstrated a role for Tregs in suppressing antigen-specific cytotoxic T-lymphocyte (CTL) responses against microglia loaded with a model peptide (SIINFEKL). We went on to show a significant decrease in the frequency of IFN-γ- and TNF-producing CD8+ T-cells when cultured with Tregs. Interestingly, a significant increase in the frequency of granzyme B- and Ki67-producing CTLs was observed. We also observed a significant decrease in the production of interleukin (IL)-6 by microglia. On further investigation, we found that Tregs significantly reduced MHC class 1 (MHC-1) expression on IFN-γ-treated microglial cells. Taken together, these studies demonstrate an immunosuppressive role for Tregs on CTL responses generated against primary microglia. Hence, modulation of Treg cell activity in combination with negative immune checkpoint blockade may stimulate anti-viral T-cell responses to more efficiently clear viral infection from microglial cell reservoirs.

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Weis-Banke, Stine Emilie, Thomas Landkildehus Lisle, Maria Perez-Penco, Aimilia Schina, Mie Linder Hübbe, Majken Siersbæk, Morten Orebo Holmström, et al. "Arginase-2-specific cytotoxic T cells specifically recognize functional regulatory T cells." Journal for ImmunoTherapy of Cancer 10, no. 10 (October 2022): e005326. http://dx.doi.org/10.1136/jitc-2022-005326.

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BackgroundHigh expression of the metabolic enzyme arginase-2 (ARG2) by cancer cells, regulatory immune cells, or cells of the tumor stroma can reduce the availability of arginine (L-Arg) in the tumor microenvironment (TME). Depletion of L-Arg has detrimental consequences for T cells and leads to T-cell dysfunction and suppression of anticancer immune responses. Previous work from our group has demonstrated the presence of proinflammatory ARG2-specific CD4 T cells that inhibited tumor growth in murine models on activation with ARG2-derived peptides. In this study, we investigated the natural occurrence of ARG2-specific CD8 T cells in both healthy donors (HDs) and patients with cancer, along with their immunomodulatory capabilities in the context of the TME.Materials and methodsA library of 15 major histocompatibility complex (MHC) class I-restricted ARG2-derived peptides were screened in HD peripheral blood mononuclear cells using interferon gamma (IFN-γ) ELISPOT. ARG2-specific CD8 T-cell responses were identified using intracellular cytokine staining and ARG2-specific CD8 T-cell cultures were established by enrichment and rapid expansion following in vitro peptide stimulation. The reactivity of the cultures toward ARG2-expressing cells, including cancer cell lines and activated regulatory T cells (Tregs), was assessed using IFN-γ ELISPOT and a chromium release assay. The Treg signature was validated based on proliferation suppression assays, flow cytometry and quantitative reverse transcription PCR (RT-qPCR). In addition, vaccinations with ARG2-derived epitopes were performed in the murine Pan02 tumor model, and induction of ARG2-specific T-cell responses was evaluated with IFN-γ ELISPOT. RNAseq and subsequent GO-term and ImmuCC analysis was performed on the tumor tissue.ResultsWe describe the existence of ARG2-specific CD8+T cells and demonstrate these CD8+T-cell responses in both HDs and patients with cancer. ARG2-specific T cells recognize and react to an ARG2-derived peptide presented in the context of HLA-B8 and exert their cytotoxic function against cancer cells with endogenous ARG2 expression. We demonstrate that ARG2-specific T cells can specifically recognize and react to activated Tregs with high ARG2 expression. Finally, we observe tumor growth suppression and antitumorigenic immunomodulation following ARG2 vaccination in an in vivo setting.ConclusionThese findings highlight the ability of ARG2-specific T cells to modulate the immunosuppressive TME and suggest that ARG2-based immunomodulatory vaccines may be an interesting option for cancer immunotherapy.

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6

Wong, Wei. "Activating T cells with asparagine." Science Signaling 14, no. 668 (February 2, 2021): eabg8244. http://dx.doi.org/10.1126/scisignal.abg8244.

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7

Olson, Matthew, and Stephen Turner. "CD4 T cells license dendritic cells to enhance polyfunctional anti-viral T helper cell responses (P6094)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 173.3. http://dx.doi.org/10.4049/jimmunol.190.supp.173.3.

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Abstract CD4 T cell help is critical for the generation of optimal B cell and CD8 T cell responses after immunization or infection. Robust and polyfunctional CD4 T cells are also generated after exposure to antigen, however, the factors that govern the development of potent CD4 T cell immunity are less clear. We demonstrate here that augmenting CD4 T cell help by adoptive transfer of increasing numbers of influenza A virus (IAV)-specific T cell receptor transgenic T cells resulted in enhanced polyclonal IAV-specific CD4 T cell responses after infection. Virus-specific CD4 T cells in mice that received augmented help also exhibited a greater capacity to produce multiple cytokines as compared to controls, indicating that CD4 T cell help is a major factor that dictates CD4 T cell polyfunctionality. Mechanistically, CD154 expression on CD4 T cells and CD40 on dendritic cells (DCs) were both necessary and sufficient to induce optimal CD4 T cell responses after infection, suggesting that helper T cells “license” DCs to enhance CD4 T cell responses. Interestingly, augmenting CD4 T cell help also resulted in enhanced IAV-specific CD4 and CD8 T cell memory responses after secondary infection. Taken together, these data define a CD4 T cell-DC circuit that promotes the priming of robust and polyfunctional CD4 T cell responses. These data also suggest that enhancing CD4 T cell help during vaccination could be used as a therapeutic approach to promote overall T cell immunity.

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8

Schilbach, Karin, Hendrik Ziegler, Jan Haarer, Marco Sterk, Hans-Georg Rammensee та Rupert Handgretinger. "Human peripheral Vδ1+ γδ T cells can develop into αβ T cells (P4460)". Journal of Immunology 190, № 1_Supplement (1 травня 2013): 52.47. http://dx.doi.org/10.4049/jimmunol.190.supp.52.47.

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Abstract The T cell compartment can be divided in two large classes: αβ and γδ T cells. It is believed that they develop in the thymus from a common progenitor and that the choice between αβ and γδ T cell fate is the first lineage decision made by progenitors after they commit to the T-cell lineage. However, here we show that peripheral Vδ1+ γδ T cells in an inflammatory environment can transdifferentiate into αβ T cells. Upon their extrathymic route of differentiation, that resembles well-characterized molecular program of thymic αβ lineage development, Vδ1+ T cells upregulate CD4+ coreceptor, develop Vδ1+ CD4+CD8+ double positive cells, show heterodimeric CD8αβ, transcribe RAG, preTα and express a particular Vβchain on their surface. Simultaneously inflammation confers controlled initiation of rearrangement in the TCRα locus. Transdifferentiation of Vδ1+ T cells at the clonal and bulk-culture level into functional CD4+ or CD8+ αβ T cells via a Vδ1+TCR/αβ+TCR double positive stage suggests that, upon inflammatory stimuli, Vδ1+ T-cell conversion participates in the induction of adaptive immune responses. Identifying an innate T cell as an αβ T-cell progenitor and showing the developmental steps linking the progenitor to adaptive, thymus-independant αβ T-cell responses as inflammatory conditions is of utmost relevance and will deeply impact evaluation of immune responses in infection, malignancy and autoimmune processes.

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9

Plitas, George, and Alexander Y. Rudensky. "Regulatory T Cells in Cancer." Annual Review of Cancer Biology 4, no. 1 (March 9, 2020): 459–77. http://dx.doi.org/10.1146/annurev-cancerbio-030419-033428.

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The immune system has evolved complex effector mechanisms to protect the host against a diversity of pathogenic organisms and regulatory adaptations that can curtail pathological sequelae of inflammatory events, prevent autoimmunity, and assist in tissue repair. Cancers, by virtue of their local manifestations of tissue dysfunction and destruction, inflammation, and genomic instability, can evoke these protective mechanisms, which support the progression of tumors and prevent their immune eradication. Central to these processes is a subset of CD4+ T cells, known as regulatory T (Treg) cells, that express the X chromosome–linked transcription factor FOXP3. In addition to their critical role in controlling autoimmunity and suppressing inflammatory responses in diverse biological settings, Treg cells are ubiquitously present in the tumor microenvironment where they promote tumor development and progression by dampening antitumor immune responses. Furthermore, Treg cells can directly support the survival of transformed cells through the elaboration of growth factors and interacting with accessory cells in tumors such as fibroblasts and endothelial cells. Current insights into the biology of tumor-associated Treg cells have opened up opportunities for their selective targeting in cancer, with the goal of alleviating their suppression of antitumor immune responses while maintaining overall immune homeostasis.

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10

Kursar, Mischo, Kerstin Bonhagen, Joachim Fensterle, Anne Köhler, Robert Hurwitz, Thomas Kamradt, Stefan H. E. Kaufmann, and Hans-Willi Mittrücker. "Regulatory CD4+CD25+ T Cells Restrict Memory CD8+ T Cell Responses." Journal of Experimental Medicine 196, no. 12 (December 9, 2002): 1585–92. http://dx.doi.org/10.1084/jem.20011347.

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CD4+ T cell help is important for the generation of CD8+ T cell responses. We used depleting anti-CD4 mAb to analyze the role of CD4+ T cells for memory CD8+ T cell responses after secondary infection of mice with the intracellular bacterium Listeria monocytogenes, or after boost immunization by specific peptide or DNA vaccination. Surprisingly, anti-CD4 mAb treatment during secondary CD8+ T cell responses markedly enlarged the population size of antigen-specific CD8+ T cells. After boost immunization with peptide or DNA, this effect was particularly profound, and antigen-specific CD8+ T cell populations were enlarged at least 10-fold. In terms of cytokine production and cytotoxicity, the enlarged CD8+ T cell population consisted of functional effector T cells. In depletion and transfer experiments, the suppressive function could be ascribed to CD4+CD25+ T cells. Our results demonstrate that CD4+ T cells control the CD8+ T cell response in two directions. Initially, they promote the generation of a CD8+ T cell responses and later they restrain the strength of the CD8+ T cell memory response. Down-modulation of CD8+ T cell responses during infection could prevent harmful consequences after eradication of the pathogen.

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11

Dhume, Kunal, Caroline Finn, Ayushi Singh, Joanne Tejero, Priyadharshini Devarajan, Susan L. Swain, and Karl Kai McKinstry. "The T-box transcription factors T-bet and Eomes repress protective Th17 CD4 T cell responses against Influenza A Virus." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 94.8. http://dx.doi.org/10.4049/jimmunol.204.supp.94.8.

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Abstract Promoting strong CD4 cell immunity is an attractive strategy to generate a universal Influenza A Virus (IAV) vaccine. Though most CD4 cell responses against IAV are classified as Th1, Th17 and cytotoxic CD4 cells (ThCTL) may also contribute to viral clearance. Interestingly, we find the transcription factor T-bet (Tbx21), the ‘master regulator’ of Th1 differentiation, to be dispensable for protective CD4 responses against IAV. Surprisingly, Tbx21−/− cells develop Th17 characteristics but retain Th1 functionality, highlighted by strong IFN-γ production. While the transcription factor Eomesodermin (Eomes) can compensate for loss of T-bet to promote antiviral CD8 responses, its roles in CD4 cells is still unclear. Here we analyze Eomes−/−, Tbx21−/− and Tbx21−/−Eomes−/− CD4 cell responses against IAV using an adoptive transfer model to determine the extent to which Eomes regulates antiviral CD4 functions. Eomes−/− cells mirrored the prototypical Th1 responses of WT CD4 cells. Strikingly, Tbx21−/−Eomes−/− cells exhibited near complete loss of both Th1 responses and ThCTL function. In contrast, Tbx21−/− Eomes−/− developed stronger Th17 attributes than Tbx21−/− cells. We assessed protection provided by transfer of in vitro Th17-primed WT, Eomes−/−, Tbx21−/− and Tbx21−/−Eomes−/− cells to unprimed WT mice infected with lethal IAV. While WT and Eomes−/− effectors gained Th1 characteristics in vivo, Tbx21−/−Eomes−/− cells strengthened their Th17 phenotype. Remarkably, all of the Th17 effectors were equally protective. Our observations reinforce the concept that Th17 cells can provide strong protection against IAV, independently of Th1 and ThCTL responses, and suggest Th17 cells use unique pathways to do so.

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12

Muul, Linda, and Fabio Candotti. "Immune Responses to Gene-Modified T Cells." Current Gene Therapy 7, no. 5 (October 1, 2007): 361–68. http://dx.doi.org/10.2174/156652307782151489.

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13

Jiang, Hong, and Leonard Chess. "Regulation of Immune Responses by T Cells." New England Journal of Medicine 354, no. 11 (March 16, 2006): 1166–76. http://dx.doi.org/10.1056/nejmra055446.

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14

Peng, Jun. "B cells help CD8+ T-cell responses." Blood 127, no. 6 (February 11, 2016): 667–69. http://dx.doi.org/10.1182/blood-2015-12-682500.

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15

Romero, Diana. "After ibrutinib, CAR T cells induce responses." Nature Reviews Clinical Oncology 14, no. 10 (August 1, 2017): 588. http://dx.doi.org/10.1038/nrclinonc.2017.124.

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Kingwell, Katie. "Engineering T cells for customized therapeutic responses." Nature Reviews Drug Discovery 15, no. 12 (November 29, 2016): 819. http://dx.doi.org/10.1038/nrd.2016.249.

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17

Shevach, Ethan M. "Control of T-cell responses by regulatory/suppressor T cells." Experimental Dermatology 12, no. 6 (December 2003): 913–14. http://dx.doi.org/10.1111/j.0906-6705.2003.0156d.x.

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Koning, F., and C. Rust. "Staphylococcal enterotoxin-mediated human T-T cell interactions." Journal of Immunology 149, no. 1 (July 1, 1992): 317–22. http://dx.doi.org/10.4049/jimmunol.149.1.317.

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Abstract Staphylococcal enterotoxins (SE) are known to stimulate a large proportion of T cells. SE bind to MHC-class II molecules on APC and a particular segment of certain TCR V beta and V gamma gene products. Resting human T cells do not express HLA class II Ag and therefore cannot present SE to T cells. Activated human T cells, however, do express HLA-DR, -DP, and -DQ Ag and could consequently serve as APC for SE. As such, local immune responses to SE might be regulated and/or abrogated by SE-mediated T-T cell interactions leading to T cell destruction. We have investigated if such SE-mediated T-T cell interactions can occur in vitro using human cytolytic TCR-alpha beta+ and TCR-gamma delta+ T cell clones. We demonstrate that the TCR-alpha beta+ T cell clones can efficiently present staphylococcal enterotoxin A (SEA) to each other: T cell clones coated with SEA are lysed by SEA-reactive T cell clones but not by a SEA-nonreactive T cell clone. Furthermore, the SEA-reactive TCR-alpha beta+ clones (but not the SEA-nonreactive clone) destruct themselves in the presence of SEA at low concentrations of SEA (less than 0.01 microgram/ml). Also, SEA-coated T cell clones can induce proliferative responses although such responses are much weaker than those induced when B cells are used as stimulator cells. In contrast, the SEA-reactive TCR-gamma delta+ T cell clones are resistant to autokilling in the presence of SEA and they do not lyse SEA-coated TCR-gamma delta+ targets. However, such targets can be lysed by TCR-alpha beta+ effector cells. These results indicate that TCR-gamma delta+ cells are relatively resistant to lysis and that during local nonspecific immune responses triggered by SE, which induces HLA-class II expression by the responding T cells, SE-mediated T-T cell interactions may play a role in the regulation and/or abrogation of these immune responses.

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19

Delon, Jérôme, Nadège Bercovici, Graça Raposo, Roland Liblau, and Alain Trautmann. "Antigen-dependent and -independent Ca2+ Responses Triggered in T Cells by Dendritic Cells Compared with B Cells." Journal of Experimental Medicine 188, no. 8 (October 19, 1998): 1473–84. http://dx.doi.org/10.1084/jem.188.8.1473.

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Dendritic cells (DCs) are much more potent antigen (Ag)-presenting cells than resting B cells for the activation of naive T cells. The mechanisms underlying this difference have been analyzed under conditions where ex vivo DCs or B cells presented known numbers of specific Ag–major histocompatibility complex (MHC) complexes to naive CD4+ T cells from T cell antigen receptor (TCR) transgenic mice. Several hundred Ag–MHC complexes presented by B cells were necessary to elicit the formation of a few T–B conjugates with small contact zones, and the resulting individual T cell Ca2+ responses were all-or-none. In contrast, Ag-specific T cell Ca2+ responses can be triggered by DCs bearing an average of 30 Ag–MHC complexes per cell. Formation of T–DC conjugates is Ag-independent, but in the presence of the Ag, the surface of the contact zone increases and so does the amplitude of the T cell Ca2+ responses. These results suggest that Ag is better recognized by T cells on DCs essentially because T–DC adhesion precedes Ag recognition, whereas T–B adhesion requires Ag recognition. Surprisingly, we also recorded small Ca2+ responses in T cells interacting with unpulsed DCs. Using DCs purified from MHC class II knockout mice, we provide evidence that this signal is mostly due to MHC–TCR interactions. Such an Ag-independent, MHC-triggered calcium response could be a survival signal that DCs but not B cells are able to deliver to naive T cells.

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20

Kedl, Ross M., William A. Rees, David A. Hildeman, Brian Schaefer, Tom Mitchell, John Kappler, and Philippa Marrack. "T Cells Compete for Access to Antigen-Bearing Antigen-Presenting Cells." Journal of Experimental Medicine 192, no. 8 (October 9, 2000): 1105–14. http://dx.doi.org/10.1084/jem.192.8.1105.

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These studies tested whether antigenic competition between T cells occurs. We generated CD8+ T cell responses in H-2b mice against the dominant ovalbumin epitope SIINFEKL (ova8) and subdominant epitope KRVVFDKL, using either vaccinia virus expressing ovalbumin (VV-ova) or peptide-pulsed dendritic cells. CD8+ T cell responses were visualized by major histocompatibility complex class I–peptide tetrameric molecules. Transfer of transgenic T cells with high affinity for ova8 (OT1 T cells) completely inhibited the response of host antigen-specific T cells to either antigen, demonstrating that T cells can directly compete with each other for response to antigen. OT1 cells also inhibited CD8+ T cell responses to an unrelated peptide, SIYRYGGL, providing it was presented on the same dendritic cells as ova8. These inhibitions were not due to a more rapid clearance of virus or antigen-presenting cells (APCs) by the OT1 cells. Rather, the inhibition was caused by competition for antigen and antigen-bearing cells, since it could be overcome by the injection of large numbers of antigen-pulsed dendritic cells. These results imply that common properties of T cell responses, such as epitope dominance and secondary response affinity maturation, are the result of competitive interactions between antigen-bearing APC and T cell subsets.

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Hiruma, K., H. Nakamura, P. A. Henkart, and R. E. Gress. "Clonal deletion of postthymic T cells: veto cells kill precursor cytotoxic T lymphocytes." Journal of Experimental Medicine 175, no. 3 (March 1, 1992): 863–68. http://dx.doi.org/10.1084/jem.175.3.863.

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Veto cell-mediated suppression of cytotoxic T lymphocyte (CTL) responses has been proposed as one mechanism by which self-tolerance is maintained in mature T cell populations. We have previously reported that murine bone marrow cells cultured in the presence of high-dose interleukin 2 (IL-2) (activated bone marrow cells [ABM]) mediate strong veto suppressor function. To examine mechanisms by which ABM may suppress precursor CTL (p-CTL) responses, we used p-CTL generated from spleen cells of transgenic mice expressing a T cell receptor specific for H-2 Ld. It was demonstrated that the cytotoxic response by these p-CTL after stimulation with irradiated H-2d/k spleen cells was suppressed by DBA/2 (H-2d) ABM, but not by B10.BR (H-2k) ABM or dm1 (Dd, Ld mutant) ABM. Flow cytometry analysis with propidium iodide staining revealed that these p-CTL were specifically deleted by incubation with H-2d ABM, but not with H-2k ABM. These data indicate that ABM veto cells kill p-CTL with specificity for antigens expressed on the surface of the ABM, and that the mechanism for veto cell activity of ABM is clonal deletion of p-CTL.

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Kerksiek, Kristen M., Dirk H. Busch, Ingrid M. Pilip, S. Elise Allen, and Eric G. Pamer. "H2-M3–Restricted T Cells in Bacterial Infection." Journal of Experimental Medicine 190, no. 2 (July 19, 1999): 195–204. http://dx.doi.org/10.1084/jem.190.2.195.

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Major histocompatibility complex (MHC) class Ib molecules have been implicated in CD8+ T cell–mediated defenses against intracellular bacterial infection, but the relative importance of MHC class Ib–restricted T cells in antimicrobial immunity is unknown. In this report, we use MHC tetramers to characterize T cell responses restricted by H2-M3, an MHC class Ib molecule that selectively presents N-formyl peptides. We find that sizeable H2-M3–restricted T cell responses, occurring earlier than MHC class Ia–restricted T cell responses, are mounted after primary infection with the intracellular bacterium Listeria monocytogenes. These H2-M3–restricted T cells are cytolytic and produce interferon γ. However, after a second L. monocytogenes infection, H2-M3–restricted memory T cell responses are minor in comparison to the much larger MHC class Ia–restricted responses. This first direct characterization of an MHC class Ib–restricted T cell response indicates that CD8+ T cells responding to L. monocytogenes infection can be divided into two groups: H2-M3–restricted responses, which provide rapid and quantitatively substantial effector function during primary infections but contribute relatively little to memory responses, and MHC class Ia–restricted responses, which expand later during primary infection but form memory T cells that respond rapidly and dramatically in response to subsequent infections by the same pathogen.

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Tsuji, Ryohei F., Marian Szczepanik, Ivana Kawikova, Vipin Paliwal, Regis A. Campos, Atsuko Itakura, Moe Akahira-Azuma, Nicole Baumgarth, Leonore A. Herzenberg, and Philip W. Askenase. "B Cell–dependent T Cell Responses." Journal of Experimental Medicine 196, no. 10 (November 11, 2002): 1277–90. http://dx.doi.org/10.1084/jem.20020649.

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Contact sensitivity (CS) is a classic example of in vivo T cell immunity in which skin sensitization with reactive hapten leads to immunized T cells, which are then recruited locally to mediate antigen-specific inflammation after subsequent skin challenge. We have previously shown that T cell recruitment in CS is triggered by local activation of complement, which generates C5a that triggers C5a receptors most likely on mast cells. Here, we show that B-1 cell–derived antihapten IgM antibodies generated within 1 day (d) of immunization combine with local challenge antigen to activate complement to recruit the T cells. These findings overturn three widely accepted immune response paradigms by showing that (a) specific IgM antibodies are required to initiate CS, which is a classical model of T cell immunity thought exclusively due to T cells, (b) CS priming induces production of specific IgM antibodies within 1 d, although primary antibody responses typically begin by day 4, and (c) B-1 cells produce the 1-d IgM response to CS priming, although these cells generally are thought to be nonresponsive to antigenic stimulation. Coupled with previous evidence, our findings indicate that the elicitation of CS is initiated by rapidly formed IgM antibodies. The IgM and challenge antigen likely form local complexes that activate complement, generating C5a, leading to local vascular activation to recruit the antigen-primed effector T cells that mediate the CS response.

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Strauss, Laura, Malgorzata Czystowska, Marta Szajnik, Magis Mandapathil, and Theresa L. Whiteside. "Differential Responses of Human Regulatory T Cells (Treg) and Effector T Cells to Rapamycin." PLoS ONE 4, no. 6 (June 22, 2009): e5994. http://dx.doi.org/10.1371/journal.pone.0005994.

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Ballesteros-Tato, André, Beatriz León, Frances E. Lund, and Troy D. Randall. "CD4+ T helper cells use CD154–CD40 interactions to counteract T reg cell–mediated suppression of CD8+ T cell responses to influenza." Journal of Experimental Medicine 210, no. 8 (July 8, 2013): 1591–601. http://dx.doi.org/10.1084/jem.20130097.

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CD4+ T cells promote CD8+ T cell priming by licensing dendritic cells (DCs) via CD40–CD154 interactions. However, the initial requirement for CD40 signaling may be replaced by the direct activation of DCs by pathogen-derived signals. Nevertheless, CD40–CD154 interactions are often required for optimal CD8+ T cell responses to pathogens for unknown reasons. Here we show that CD40 signaling is required to prevent the premature contraction of the influenza-specific CD8+ T cell response. CD40 is required on DCs but not on B cells or T cells, whereas CD154 is required on CD4+ T cells but not CD8+ T cells, NKT cells, or DCs. Paradoxically, even though CD154-expressing CD4+ T cells are required for robust CD8+ T cell responses, primary CD8+ T cell responses are apparently normal in the absence of CD4+ T cells. We resolved this paradox by showing that the interaction of CD40-bearing DCs with CD154-expressing CD4+ T cells precludes regulatory T cell (T reg cell)–mediated suppression and prevents premature contraction of the influenza-specific CD8+ T cell response. Thus, CD4+ T helper cells are not required for robust CD8+ T cell responses to influenza when T reg cells are absent.

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Rivera, Amariliz, Tobias M. Hohl, Nichole Collins, Ingrid Leiner, Alena Gallegos, Shinobu Saijo, Jesse W. Coward, Yoichiro Iwakura, and Eric G. Pamer. "Dectin-1 diversifies Aspergillus fumigatus–specific T cell responses by inhibiting T helper type 1 CD4 T cell differentiation." Journal of Experimental Medicine 208, no. 2 (January 17, 2011): 369–81. http://dx.doi.org/10.1084/jem.20100906.

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Анотація:

Pulmonary infection of mice with Aspergillus fumigatus induces concurrent T helper type 1 (Th1) and Th17 responses that depend on Toll-like receptor/MyD88 and Dectin-1, respectively. However, the mechanisms balancing Th1 and Th17 CD4 T cell populations during infection remain incompletely defined. In this study, we show that Dectin-1 deficiency disproportionally increases Th1 responses and decreases Th17 differentiation after A. fumigatus infection. Dectin-1 signaling in A. fumigatus–infected wild-type mice reduces IFN-γ and IL-12p40 expression in the lung, thereby decreasing T-bet expression in responding CD4 T cells and enhancing Th17 responses. Absence of IFN-γ or IL-12p35 in infected mice or T-bet in responding CD4 T cells enhances Th17 differentiation, independent of Dectin-1 expression, in A. fumigatus–infected mice. Transient deletion of monocyte-derived dendritic cells also reduces Th1 and boosts Th17 differentiation of A. fumigatus–specific CD4 T cells. Our findings indicate that Dectin-1–mediated signals alter CD4 T cell responses to fungal infection by decreasing the production of IL-12 and IFN-γ in innate cells, thereby decreasing T-bet expression in A. fumigatus–specific CD4 T cells and enabling Th17 differentiation.

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James, Edd, Ian Bailey, Emma Reeves, and Tim Elliott. "Differential T cell suppression through regulatory T cells (66.43)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 66.43. http://dx.doi.org/10.4049/jimmunol.186.supp.66.43.

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Abstract Depletion of regulatory T cells in the CT26 murine tumour model stimulates a robust protective T cell response which is also protective to challenge with other tumours of different histological origins. We have characterised a cross-protective antigen, GSW11 (GGPESFYCASW) presented by H-2Dd. This antigen was found to be encoded within the env (gp90) gene of an endogenous retrovirus emv-1 (MuLV), previously shown to encode other CT26 antigens. Further characterisation of GSW11-specific T cell responses has shown them to be suppressed by Tregs and are absent in CT26 challenged mice. In comparison, AH1-specific T cells (AH1 is a previously characterised CT26 antigen) are not suppressed. Here we show that the GSW11-specific T cell responses are present in CT26 challenged Treg replete mice for a limited period in the tumour of challenged mice. Characterisation of the AH1 and GSW11-specific T cells infiltrating the CT26 tumour reveal differences in expression of several molecules associated with cell survival and activation. These expression profiles provide an intriguing explanation for the differential suppression of tumour-specific T cells in vivo.

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DeKruyff, R. H., C. Clayberger, and H. Cantor. "Monoclonal helper T cells induce B cell responses to T-independent antigens: antigen-specific T cells are directly stimulated by activated B cells in the absence of antigen." Journal of Immunology 134, no. 1 (January 1, 1985): 86–90. http://dx.doi.org/10.4049/jimmunol.134.1.86.

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Abstract Efficient B cell responses to most polysaccharide antigens such as TNP-PAA or TNP-Ficoll require factors produced by activated T cells. However, the mechanism of T cell activation during such responses has not been established, because these antigens do not activate T cells, either directly or in conjunction with I-A gene products. We used a panel of antigen-specific monoclonal helper T cells to study T cell activation during the course of such responses. We show that activated I-A-identical B cells directly stimulate these monoclonal T cells, and that this stimulation is in the absence of nominal antigen. The high frequency of inducer cells that are stimulated by activated B cells suggests a major biologic role for this novel pathway of T cell activation.

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29

Gigley, Jason P., Daria L. Ivanova, and Stephen L. Denton. "NKp46+ NK cells regulate brain CD4+ T cells to promote chronic Toxoplasma gondii infection." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 190.72. http://dx.doi.org/10.4049/jimmunol.202.supp.190.72.

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Abstract Reactivation of chronic Toxoplasma gondii (T. gondii) infection and toxoplasmic encephalitis is a major health concern in immune compromised people. Dysregulated T-cell responses are thought to promote chronic Toxoplasmosis. The non-T-cell factors that contribute to T cell dysregulation and chronic T. gondii infection are unclear. We have discovered that NKp46+ NK cells paradoxically increase the frequency and number of IFNγ+TNFα+CD4+ T-cells in the brain in during chronic T. gondii infection. Depletion of NK cells resulted in a decrease in polyfunctional brain CD4+ T-cells and an increase in IFNγ+Grzb+CD8+ T-cell responses in the brain. This decrease in CD4+ T-cell and increase in CD8+ T-cell responses correlated with better survival of chronically infected mice. This result suggests that NKp46+ NK cells drive an NK cell-dependent CD4+ T cell response that is detrimental to the CD8+ T cell response important for controlling chronic T. gondii infection. In support of this possibility, adoptive transfer of NK cell-dependent CD4+ T cells into chronically infected mice reduced polyfunctional CD8+ T-cell responses in the brain while CD4+ T cells generated in the absence of NK cells during chronic T. gondii infection did not. NKp46+ NK cells were not found in brain tissue, but appear to localize to the vasculature of the brain and periphery during chronic T. gondii infection. Surprisingly, we observe that NKp46+ NK cells increase their expression of MHC Class II. Our results lead us to hypothesize that during chronic T. gondii infection NKp46+ NK cells acquire the ability to prime CD4+ T-cell responses via MHC Class II expression resulting in decreased polyfunctional CD8 T cell responses to promote parasite persistence.

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Thompson, Scott Beckett, Daria Leonidovna Ivanova, Jared Klarquist, James Scott-Browne, and Ross M. Kedl. "Vaccine-elicited T cells rely on a distinct transcriptional program from infection-elicited T cells." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 166.18. http://dx.doi.org/10.4049/jimmunol.204.supp.166.18.

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Abstract Protection from pathogens relies on both humoral (antibody-mediated) and cellular (T cell-mediated) responses. While infections robustly elicit both of these types of immunity, currently approved vaccine adjuvants largely fail to induce significant T cell responses. However, recent work by our lab and others suggests that the mechanisms governing vaccine-elicited T cells (Tvac) may be substantially different than those governing infection-elicited T cells (Tinf). We have recently demonstrated that optimal subunit vaccine-elicited T cell responses rely on different cytokine signals (IL-27 and 15) and metabolic function (oxidative phosphorylation vs. aerobic glycolysis) leading to phenotypically and functionally different outcomes (memory vs. effector). Our goal was to investigate the transcriptional programming that promotes Tvac formation. Using a combined ATACseq, bulk RNA-seq and single-cell RNA-seq approach, we compared Tvac and Tinf at various time points post-immunization or infectious challenge. Our data indicate that the chromatin organization and gene expression of Tvac markedly diverges from Tinf even at early time points. Furthermore, single-cell analysis indicates that Tvac represent a unique subset of activated/memory T cells, distinct from Tinf. Remarkably, while displaying a gene signature similar to highly proliferative cells, Tvac also share transcriptional properties with recently identified stem cell memory T cells, such as oxidative phosphorylation and transcription factor TCF1 gene signatures. Taken together, our data have identified a novel transcriptional program that supports a robust vaccine-elicited T cell response with implications for future therapeutic vaccine design.

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Xiang, Jim. "DIRECT ORCHESTRATION OF CD8+ T-KILLERS BY CD4+ T-HELPERS AND CD+ T-LICENSED ANTIGEN PRESENTING CELLS (130.33)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 130.33. http://dx.doi.org/10.4049/jimmunol.184.supp.130.33.

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Abstract We previously proposed a CD4+ Th-APC concept by demonstrating that in vitro ovalbumin (OVA)-pulsed dendritic cell (DCova)-activated CD4+ T cells acquired peptide/major histocompatibility complex (pMHC) I from DCova and are capable of stimulating CD8+ cytotoxic T lymphocytes (CTLs). In this study, we developed a novel immunization protocol to “dissect apart” respective roles of DCova, CD4+ and CD8+ T cells separately in an in vivo environment with close to physiological condition. We first used anti-CD4 and anti-CD8 antibody (Ab) and deptheria toxin (DT) for in vivo depletion of CD4+ and CD8+ T cells and DCova derived from DT receptor (DTR)-CD11c transgenic mice, respectively, at different time points of the protocol. We then assessed the priming of CD8+ CTL responses in blood using FITC-CD8 and PE-Kb/OVA257-264 tetramer staining by flow cytometry. We found that (i) mice that have CD4+ T-licensed DCova but lack CD4+ T cells by anti-CD4 Ab treatment during CD8+ CTL priming, induced CTL effector/memory responses, (ii) CD4+ T cells with in vivo acquired pMHC I, but not those without pMHC I acquisition stimulated CTL responses, and (iii) APC-primed CD4+ T cells mounted more efficient CTL effector/memory responses than CD4+ T-licensed DCova. Our results thus provide a clear in vivo evidence for a direct orchestration of CD8+ T-killers by CD4+ T-helpers and CD4+ T-licensed APCs. This conceptual advance may have great impacts in re-evaluation of antitumor and autoimmune responses.

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32

Schütz, Christian, Martin Fleck, Andreas Mackensen, Alessia Zoso, Dagmar Halbritter, Jonathan P. Schneck, and Mathias Oelke. "Killer artificial antigen-presenting cells: a novel strategy to delete specific T cells." Blood 111, no. 7 (April 1, 2008): 3546–52. http://dx.doi.org/10.1182/blood-2007-09-113522.

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Abstract Several cell-based immunotherapy strategies have been developed to specifically modulate T cell–mediated immune responses. These methods frequently rely on the utilization of tolerogenic cell–based antigen-presenting cells (APCs). However, APCs are highly sensitive to cytotoxic T-cell responses, thus limiting their therapeutic capacity. Here, we describe a novel bead-based approach to modulate T-cell responses in an antigen-specific fashion. We have generated killer artificial APCs (κaAPCs) by coupling an apoptosis-inducing α-Fas (CD95) IgM mAb together with HLA-A2 Ig molecules onto beads. These κaAPCs deplete targeted antigen-specific T cells in a Fas/Fas ligand (FasL)–dependent fashion. T-cell depletion in cocultures is rapidly initiated (30 minutes), dependent on the amount of κaAPCs and independent of activation-induced cell death (AICD). κaAPCs represent a novel technology that can control T cell–mediated immune responses, and therefore has potential for use in treatment of autoimmune diseases and allograft rejection.

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33

Hope, Jennifer L., Christopher Stairiker, Panagiota Spantidea, Donald Tom Gracias, Alison J. Carey, Marjan van Meurs, Inge Brouwers-Haspels, et al. "MicroRNA-155 regulates T-bet expression in anti-viral CD8+ T cells." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 121.5. http://dx.doi.org/10.4049/jimmunol.198.supp.121.5.

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Abstract MicroRNAs (miRNAs) are small, single-stranded non-coding RNAs that play essential roles in regulating key cellular processes, and are highly conserved across species. miRNA are known to regulate immune cells and play an important role in effective CD8+ T cell (CTL) responses to viral infection and tumors. To understand the role of miRNA in CTL responses we performed microarray miRNA expression profiling and identified unique in vivo expression patterns of miRNAs in naïve and effector anti-viral CTL. In particular, miR-155, which we and others previously have demonstrated to regulate CTL responses, was significantly upregulated in effector CTL. We show that further increasing the levels of miR-155 by retroviral overexpression significantly augments anti-viral effector CTL and skews memory CD8+ T cells towards an effector memory phenotype. MiR-155 overexpression resulted in enhanced T-bet expression, which is known to be required for effector CTL and to promote effector memory cell formation. MiR-155 overexpression-induced T-bet expression was required for miR-155 mediated increases in effector CTL. Our studies have revealed an important and unexpected link between miR-155 and T-bet transcription factor in the context of in vivo CTL responses.

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34

Brandes, M., K. Willimann, G. Bioley, N. Levy, M. Eberl, M. Luo, R. Tampe, F. Levy, P. Romero, and B. Moser. "Cross-presenting human T cells induce robust CD8+ T cell responses." Proceedings of the National Academy of Sciences 106, no. 7 (January 26, 2009): 2307–12. http://dx.doi.org/10.1073/pnas.0810059106.

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35

Kelso, A. "Educating T cells: Development and reversal of T cell cytokine responses." Journal of Neuroimmunology 90, no. 1 (September 1998): 7. http://dx.doi.org/10.1016/s0165-5728(98)91233-4.

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36

Kubo, Masato. "T follicular helper and T H 2 cells in allergic responses." Allergology International 66, no. 3 (July 2017): 377–81. http://dx.doi.org/10.1016/j.alit.2017.04.006.

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37

Janeway, Jr, C. "Responses of T cells to ligands for the T-cell receptor." Seminars in Immunology 8, no. 2 (April 1996): 109–15. http://dx.doi.org/10.1006/smim.1996.0013.

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38

Krug, Anne, Ravi Veeraswamy, Andrew Pekosz, Osami Kanagawa, Emil R. Unanue, Marco Colonna, and Marina Cella. "Interferon-producing Cells Fail to Induce Proliferation of Naive T Cells but Can Promote Expansion and T Helper 1 Differentiation of Antigen-experienced Unpolarized T Cells." Journal of Experimental Medicine 197, no. 7 (March 31, 2003): 899–906. http://dx.doi.org/10.1084/jem.20021091.

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Interferon-producing cells (IPCs) secrete high levels of type I interferon in response to certain viruses. The lack of lineage markers, the expression of major histocompatibility complex (MHC) class II and the capacity to stimulate allogeneic T cells have led these cells to be classified as a subset of dendritic cells (DCs), called plasmacytoid DCs (PDCs). However, the role of IPCs/PDCs in initiating primary immune responses remains elusive. Here we examined the antigen presenting capacity of murine IPCs in antigen specific systems. While CD8α+ and CD11b+ DCs induced logarithmic expansion of naive CD4 and CD8 T cells, without conferring T helper commitment at a first encounter, primary IPCs lacked the ability to stimulate naive T cells. However, when antigen-experienced, nonpolarized T cells expanded by classical DC subsets, were restimulated by IPCs, they proliferated and produced high amounts of IFN-γ. These data indicate that IPCs can effectively stimulate preactivated or memory-type T cells and exert an immune-regulatory role. They also suggest that expansion of naive T cells and acquisition of effector function during antigen-specific T cell responses may involve different antigen-presenting cell (APC) types. Independent and coordinated control of T cell proliferation and differentiation would provide the immune system with greater flexibility in regulating immune responses.

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39

Hiwarkar, Prashant, Waseem Qasim, Ida Ricciardelli, Kimberly Gilmour, Sergio Quezada, Aurore Saudemont, Persis Amrolia, and Paul Veys. "Cord blood T cells mediate enhanced antitumor effects compared with adult peripheral blood T cells." Blood 126, no. 26 (December 24, 2015): 2882–91. http://dx.doi.org/10.1182/blood-2015-06-654780.

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Key Points CB T cells mediate enhanced antitumor responses compared with PB T cells in a murine model of B-cell lymphoma. The antitumor activity correlates with increased tumor-homing of CCR7high CB CD8+ T cells and rapid gain of cytotoxic and Th1 function.

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40

Brody, Joshua D., Matthew J. Goldstein, Debra K. Czerwinski, and Ronald Levy. "Immunotransplantation preferentially expands T-effector cells over T-regulatory cells and cures large lymphoma tumors." Blood 113, no. 1 (January 1, 2009): 85–94. http://dx.doi.org/10.1182/blood-2008-05-155457.

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Abstract Ex vivo–expanded tumor-infiltrating lymphocytes infused into lymphodepleted recipients has clear antitumor efficacy. More practical sources of such antitumor lymphocytes would broaden the application of this approach. Previously, we described an in situ vaccination combining chemotherapy with intratumoral injection of CpG-enriched oligonucleotides, which induced T-cell immunity against established lymphoma. An ongoing clinical trial of this maneuver has demonstrated clinical responses in lymphoma patients. Here, we use this vaccine maneuver to generate immune cells for transfer into irradiated, syngeneic recipients. Transferred tumor-specific T-effector (Teff) cells preferentially expanded, increasing the Teff/T-regulatory (Treg) ratio in these “immunotransplantation” recipients and curing large and metastatic tumors. Donor T cells were necessary for tumor protection, and CD8 T-cell immune responses were enhanced by posttransplantation booster vaccination. Hematopoietic stem cell transplantation is a standard therapy for lymphoma. Therefore, in situ tumor vaccination followed by immunotransplantation of harvested tumor-specific T cells could be directly tested in clinical trials to treat otherwise resistant malignancies.

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Sapoznikov, Anita, Jens A. A. Fischer, Tami Zaft, Rita Krauthgamer, Andrzej Dzionek, and Steffen Jung. "Organ-dependent in vivo priming of naive CD4+,but not CD8+,T cells by plasmacytoid dendritic cells." Journal of Experimental Medicine 204, no. 8 (July 23, 2007): 1923–33. http://dx.doi.org/10.1084/jem.20062373.

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Plasmacytoid dendritic cells (PDCs) play a pivotal role as cytokine-secreting accessory cells in the antimicrobial immune defense. In contrast, the capacity of PDCs to act as antigen-presenting cells in naive T cell priming remains unclear. By studying T cell responses in mice that lack conventional DCs (cDCs), and by the use of a PDC-specific antigen-targeting strategy, we show that PDCs can initiate productive naive CD4+ T cell responses in lymph nodes, but not in the spleen. PDC-triggered CD4+ T cell responses differed from cDC-driven responses in that they were not associated with concomitant CD8+ T cell priming. Our results establish PDCs as a bona fide DC subset that initiates unique CD4+ Th cell–dominated primary immune responses.

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Yeh, Chen-Hao, Masayuki Kuraoka, Heather Lynch, Gregory D. Sempowski, and Garnett H. Kelsoe. "TCR Repertoire Analysis of Mouse T Follicular Helper Cells and T Follicular Regulatory Cells Following Immunization." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 133.37. http://dx.doi.org/10.4049/jimmunol.196.supp.133.37.

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Abstract Generation of high-affinity and class-switched antibody requires the germinal center (GC) reaction after infection or immunization. Within the B-cell follicles of secondary lymphoid organs, the GC represents a sophisticated collaboration between antigen-specific B cells, follicular dendritic cells, T follicular helper (TFH) cells and T follicular regulatory (TFREG) cells. Despite intensive interest in the development and effector function of TFH and TFREG cells, little is known regarding the selection of T-cell receptor (TCR) repertoire during polyclonal GC reactions. In order to evaluate native, polyclonal TCR responses elicited by a complex antigen, we developed a sorting strategy to isolate TFH/TFREG cell populations that were activated and expanded after s.c. immunization with NP15-OVA. TCRβ VDJ rearrangements were recovered from highly purified TCRβ+CD4+CXCR5hiPD-1+Bcl-6+FoxP3− TFH cells and TCRβ+CD4+ CXCR5hiPD-1+Bcl-6+FoxP3+ TFREG cells, amplified by PCR, and sequenced. Analysis of the antigen-specific TCR repertoire of TFH/TFREG cells provides important insights into the factors influencing T-cell recruitment and clonal expansion following infection or vaccination, especially when linked to contemporary analysis of the GC B-cell repertoire. These findings may inform rational and selective control strategy of the GC reaction. Vaccine development can accordingly focus on modulating TFH/TFREG responses to facilitate optimal adaptive immune responses.

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Ptak, W., and P. W. Askenase. "Gamma delta T cells assist alpha beta T cells in adoptive transfer of contact sensitivity." Journal of Immunology 149, no. 11 (December 1, 1992): 3503–8. http://dx.doi.org/10.4049/jimmunol.149.11.3503.

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Abstract Cutaneous immune responses to contact sensitizers such as picryl chloride or oxazolone, are classical manifestations of T cell-mediated immunity in vivo. In fact, the first documentation of T cell-mediated immunity was the ability to adoptively transfer contact sensitivity (CS) responses. Although it is now clear that Ag/MHC-restricted alpha beta TCR positive effector T cells are responsible for 24 to 48 h CS responses, other subsets of Thy-1+ cells in mice also participate in the elicitation of CS. Thus, Thy-1+, CD5+, CD3-, B220+, hapten-specific, non-MHC-restricted early-acting cells are required to initiate CS responses by leading to local serotonin release, which allows for extravascular recruitment of the late-acting, alpha beta TCR+, CS effector T cells. This study describes another T cell population that is needed for the adoptive transfer of CS by alpha beta T cells. In vitro treatment of a mixture of CS effector cells with hamster mAb to gamma delta TCR, together with rabbit complement, or by panning on anti-hamster Ig-coated dishes, diminished substantially the subsequent transfer of CS reactivity without affecting either CS-initiating cells, or the later-acting, alpha beta TCR+ CS effector T cells. Immune cells treated with anti-alpha beta TCR mAb, or recovered as adherent cells from petri dishes after anti-gamma delta TCR panning (i.e., gamma delta TCR-enriched cells), reconstituted the ability of anti-gamma delta TCR-treated immune cells (i.e., alpha beta TCR-enriched cells) to transfer 24-h CS responsiveness. The phenotype of the gamma delta T cells that assisted CS effector alpha beta T cells was: CD3+, CD4-, and CD8+. The gamma delta T cells that assisted alpha beta T cells were not Ag-specific since anti-alpha beta-TCR-treated cells (gamma delta T-enriched) from picryl chloride immunized donors aided alpha beta T cells (anti-gamma delta TCR-treated) from oxazolone-immunized donors, and conversely gamma delta T cells from oxazolone-immunized donors aided alpha beta T cells from picryl chloride immunized donors. Furthermore, the CS-regulating gamma delta T cells were not MHC-restricted because gamma delta T cells from H2d or H2b donors could assist alpha beta T cells from H2k donors. It was concluded that a regulatory population of non-Ag specific, non-MHC-restricted gamma delta T cells was needed to assist immune effector, Ag/MHC-specific alpha beta T cells in the adoptive transfer of CS.

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Aandahl, Einar M., Jakob Michaëlsson, Walter J. Moretto, Frederick M. Hecht, and Douglas F. Nixon. "Human CD4+ CD25+ Regulatory T Cells Control T-Cell Responses to Human Immunodeficiency Virus and Cytomegalovirus Antigens." Journal of Virology 78, no. 5 (March 1, 2004): 2454–59. http://dx.doi.org/10.1128/jvi.78.5.2454-2459.2004.

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ABSTRACT Regulatory T (TR) cells maintain tolerance to self-antigens and control immune responses to alloantigens after organ transplantation. Here, we show that CD4+ CD25+ human TR cells suppress virus-specific T-cell responses. Depletion of TR cells from peripheral blood mononuclear cells enhances T-cell responses to cytomegalovirus and human immunodeficiency virus antigens. We propose that chronic viral infections lead to induction of suppressive TR cells that inhibit the antiviral immune response.

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45

Noble, Alistair, Lydia Durant, Lesley Hoyles, Anne L. Mccartney, Ripple Man, Jonathan Segal, Samuel P. Costello, et al. "Deficient Resident Memory T Cell and CD8 T Cell Response to Commensals in Inflammatory Bowel Disease." Journal of Crohn's and Colitis 14, no. 4 (October 26, 2019): 525–37. http://dx.doi.org/10.1093/ecco-jcc/jjz175.

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Abstract Background and Aims The intestinal microbiota is closely associated with resident memory lymphocytes in mucosal tissue. We sought to understand how acquired cellular and humoral immunity to the microbiota differ in health versus inflammatory bowel disease [IBD]. Methods Resident memory T cells [Trm] in colonic biopsies and local antibody responses to intraepithelial microbes were analysed. Systemic antigen-specific immune T and B cell memory to a panel of commensal microbes was assessed. Results Systemically, healthy blood showed CD4 and occasional CD8 memory T cell responses to selected intestinal bacteria, but few memory B cell responses. In IBD, CD8 memory T cell responses decreased although B cell responses and circulating plasmablasts increased. Possibly secondary to loss of systemic CD8 T cell responses in IBD, dramatically reduced numbers of mucosal CD8+ Trm and γδ T cells were observed. IgA responses to intraepithelial bacteria were increased. Colonic Trm expressed CD39 and CD73 ectonucleotidases, characteristic of regulatory T cells. Cytokines/factors required for Trm differentiation were identified, and in vitro-generated Trm expressed regulatory T cell function via CD39. Cognate interaction between T cells and dendritic cells induced T-bet expression in dendritic cells, a key mechanism in regulating cell-mediated mucosal responses. Conclusions A previously unrecognised imbalance exists between cellular and humoral immunity to the microbiota in IBD, with loss of mucosal T cell-mediated barrier immunity and uncontrolled antibody responses. Regulatory function of Trm may explain their association with intestinal health. Promoting Trm and their interaction with dendritic cells, rather than immunosuppression, may reinforce tissue immunity, improve barrier function, and prevent B cell dysfunction in microbiota-associated disease and IBD aetiology.

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Oh, Sejin, and Se-ho Park. "NKT cells act as helper T cells to cytotoxic T cells by direct recognition of CD1d on T cells (IRC8P.487)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 190.15. http://dx.doi.org/10.4049/jimmunol.192.supp.190.15.

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Abstract Cytotoxic T lymphocytes (CTLs), known as CD8+ T cells, recognize their targets by binding to antigens associated with MHC class I. NKT cells recognize foreign glycolipid antigens and endogenous glycolipid antigens presented by CD1d which is an MHC class I- like molecule. NKT cells have been shown to be essential for the optimal activation of CTLs. In this study, we investigated the mechanism how NKT cells provide help for the CTL responses. We observed significantly higher production of IFN-γ by antigen-stimulated OT-1 CD8+ T cells in the presence of NKT cells. This enhanced CTL activation by NKT cells was observed even in the antigen presenting cell (APC)-free conditions. We also found that CD8+ T cells start to up-regulate surface expression of CD1d reaching highest level at around 18 hours upon antigen recognition. These results suggest that not only APC, but also activated CTLs receive direct help from NKT cells by increasing CD1d expression on their cell surface when they recognize cognate antigens.

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47

A. Barr, Tom, Mohini Gray, and David Gray. "B Cells: Programmers of CD4 T Cell Responses." Infectious Disorders - Drug Targets 12, no. 3 (May 1, 2012): 222–31. http://dx.doi.org/10.2174/187152612800564446.

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48

Sakaguchi, Shimon. "Control of Immune Responses by Regulatory T Cells." Rheumatology 56, suppl_3 (March 2017): iii2. http://dx.doi.org/10.1093/rheumatology/kex147.

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49

Finnegan, Alison, Barbara White Needleman, and Richard J. Hodes. "Function of Autoreactive T Cells in Immune Responses." Immunological Reviews 116, no. 1 (August 1990): 15–31. http://dx.doi.org/10.1111/j.1600-065x.1990.tb00802.x.

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Sayed, Blayne Amir, and Melissa A. Brown. "Mast cells as modulators of T-cell responses." Immunological Reviews 217, no. 1 (June 2007): 53–64. http://dx.doi.org/10.1111/j.1600-065x.2007.00524.x.

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