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Journal articles on the topic 'Immune humoral response'

Author: Grafiati

Published: 25 May 2024

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1

Banerjee, Dilip K., and G. Richard Hilson. "Humoral immune response in infection." Current Opinion in Infectious Diseases 4, no. 3 (June 1991): 325–31. http://dx.doi.org/10.1097/00001432-199106000-00011.

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2

Ye, Jianmin, Ilsa M. Kaattari, Cuiyan Ma, and Stephen Kaattari. "The teleost humoral immune response." Fish & Shellfish Immunology 35, no. 6 (December 2013): 1719–28. http://dx.doi.org/10.1016/j.fsi.2013.10.015.

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3

Skerra, A. "Imitating the humoral immune response." Current Opinion in Chemical Biology 7, no. 6 (December 2003): 683–93. http://dx.doi.org/10.1016/j.cbpa.2003.10.012.

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4

YANG, HYUN MO. "A MATHEMATICAL MODEL TO ASSESS THE IMMUNE RESPONSE AGAINSTTRYPANOSOMA CRUZIINFECTION." Journal of Biological Systems 23, no. 01 (March 2015): 131–63. http://dx.doi.org/10.1142/s0218339015500084.

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A mathematical model is developed to assess humoral and cellular immune responses against Trypanosoma cruzi infection. Analysis of the model shows a unique non-trivial equilibrium, which is locally asymptotically stable, except in the case of a strong cellular response. When the proliferation of the activated CD8 T cells is increased, this equilibrium becomes unstable and a limit cycle appears. However, this behavior can be avoided by increasing the action of the humoral response. Therefore, unbalanced humoral and cellular responses can be responsible for long asymptomatic period, and the control of Trypanosoma cruzi infection is a consequence of well coordinated action of both humoral and cellular responses.

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5

Palosuo, Tima, and Kimmo Aho. "Humoral Immune Response to Mammalian Allergens." Allergy and Asthma Proceedings 8, no. 4 (July 1, 1987): 233–35. http://dx.doi.org/10.2500/108854187779032460.

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6

C, Prabha, Kripa V., and Sulochana D. Das. "Humoral Immune Response in Tuberculous Pleuritis." American Journal of Immunology 1, no. 2 (February 1, 2005): 68–73. http://dx.doi.org/10.3844/ajisp.2005.68.73.

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7

van Spriel, Annemiek B. "Tetraspanins in the humoral immune response." Biochemical Society Transactions 39, no. 2 (March 22, 2011): 512–17. http://dx.doi.org/10.1042/bst0390512.

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The tetraspanins represent a large superfamily of four-transmembrane proteins that are expressed on all nucleated cells. Tetraspanins play a prominent role in the organization of the plasma membrane by co-ordinating the spatial localization of transmembrane proteins and signalling molecules into ‘tetraspanin microdomains’. In immune cells, tetraspanins interact with key leucocyte receptors [including MHC molecules, integrins, CD4/CD8 and the BCR (B-cell receptor) complex] and as such can modulate leucocyte receptor activation and downstream signalling pathways. There is now ample evidence that tetraspanins on B-lymphocytes are important in controlling antibody production. The tetraspanin CD81 interacts with the BCR complex and is critical for CD19 expression and IgG production, whereas the tetraspanin CD37 inhibits IgA production and is important for IgG production. By contrast, the tetraspanins CD9, Tssc6 and CD151 appear dispensable for humoral immune responses. Thus individual tetraspanin family members have specific functions in B-cell biology, which is evidenced by recent studies in tetraspanin-deficient mice and humans. The present review focuses on tetraspanins expressed by B-lymphocytes and discusses novel insights into the function of tetraspanins in the humoral immune response.

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8

Brooks, G. F., and C. J. Lammel. "Humoral immune response to gonococcal infections." Clinical Microbiology Reviews 2, Suppl (April 1989): S5–10. http://dx.doi.org/10.1128/cmr.2.suppl.s5.

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9

Brooks, G. F., and C. J. Lammel. "Humoral immune response to gonococcal infections." Clinical Microbiology Reviews 2, Suppl (1989): S5–10. http://dx.doi.org/10.1128/cmr.2.suppl.s5-10.1989.

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10

Grimaldi, M. E., A. Lazzarin, A. Castagna, and N. Canal. "Humoral immune response following HIV infection." Acta Neurologica Scandinavica 79, no. 3 (March 1989): 258. http://dx.doi.org/10.1111/j.1600-0404.1989.tb03762.x.

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11

Calvanico, Nickolas J. "The Humoral Immune Response in Autoimmunity." Dermatologic Clinics 11, no. 3 (July 1993): 379–89. http://dx.doi.org/10.1016/s0733-8635(18)30237-7.

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12

Fleisher, Gary R., Marjeanne Collins, and Samuel Fager. "Humoral immune response in infectious mononucleosis." Journal of Adolescent Health Care 6, no. 6 (November 1985): 424–28. http://dx.doi.org/10.1016/s0197-0070(85)80046-2.

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13

KONRADSEN, HELLE BOSSEN. "Humoral immune response to pneumococcal vaccination." APMIS 104, S60 (June 1996): 5–28. http://dx.doi.org/10.1111/j.1600-0463.1996.tb05577.x.

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14

Shishido, Stephanie N., Sriram Varahan, Kai Yuan, Xiangdong Li, and Sherry D. Fleming. "Humoral innate immune response and disease." Clinical Immunology 144, no. 2 (August 2012): 142–58. http://dx.doi.org/10.1016/j.clim.2012.06.002.

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15

DESCHEERDER, I. "Humoral immune response during acute myocarditis." Journal of Molecular and Cellular Cardiology 21 (July 1989): S70. http://dx.doi.org/10.1016/0022-2828(89)91420-x.

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16

Chiaramonte, M., and R. Russo. "The echinoderm innate humoral immune response." Italian Journal of Zoology 82, no. 3 (July 2015): 300–308. http://dx.doi.org/10.1080/11250003.2015.1061615.

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17

Kelsoe, Garnett. "Studies of the Humoral Immune Response." Immunologic Research 22, no. 2-3 (2000): 199–210. http://dx.doi.org/10.1385/ir:22:2-3:199.

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18

Galkin, O. Yu, A. G. Komar, and O. B. Besarab. "Different mice inbred strains humoral immune response against human prostate-specific antigen." Ukrainian Biochemical Journal 91, no. 1 (January 28, 2019): 30–37. http://dx.doi.org/10.15407/ubj91.01.030.

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19

Widodo, Trijoedani. "Respons imun humoral pada pulpitis (Humoral immune response on pulpitis)." Dental Journal (Majalah Kedokteran Gigi) 38, no. 2 (June 1, 2005): 49. http://dx.doi.org/10.20473/j.djmkg.v38.i2.p49-51.

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20

Yousif, Ashraf S., Tatsushi Omatsu, Grant Weaver, Pankaj Shah, Hans-Christian Reinnecker, and Daniel Lingwood. "Cellular gatekeepers of the humoral immune response." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 211.12. http://dx.doi.org/10.4049/jimmunol.198.supp.211.12.

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Abstract The spleen is critical for eliminating bloodborne pathogens and preventing systemic infection. In the marginal zone (MZ), the site in which splenic antibody responses are first initiated, we have discovered a dendritic cell (DC) ‘hairnet’ architecture that is responsible for extracting two unrelated viral antigens from the perfusing blood and importing them into B cell follicle to initiate IgM and IgG responses. The IgM response was independent of T-cell help, and proceeded via DC display of conformationally intact antigen in the absence of MHC proteins. Interestingly the DC-antigen captures and importing mechanism are solely governed by the glycan of the antigens. Taking all together, we propose that DC hairnet architecture, inshealthing the MZ, constitutes a filtering device that capture and concentrates protein antigens in a glycan-dependent manner from solution and catalyzes their delivery to B cells follicle to initiate humoral immune responses.

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21

Schietzel, Simeon, Manuel Anderegg, Andreas Limacher, Alexander Born, Michael P. Horn, Britta Maurer, Cedric Hirzel, Daniel Sidler, and Matthias B. Moor. "Humoral and cellular immune responses on SARS-CoV-2 vaccines in patients with anti-CD20 therapies: a systematic review and meta-analysis of 1342 patients." RMD Open 8, no. 1 (February 2022): e002036. http://dx.doi.org/10.1136/rmdopen-2021-002036.

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BackgroundImmune responses on SARS-CoV-2 vaccination in patients receiving anti-CD20 therapies are impaired but vary considerably. We conducted a systematic review and meta-analysis of the literature on SARS-CoV-2 vaccine induced humoral and cell-mediated immune response in patients previously treated with anti-CD20 antibodies.MethodsWe searched PubMed, Embase, Medrxiv and SSRN using variations of search terms ‘anti-CD20’, ‘vaccine’ and ‘COVID’ and included original studies up to 21 August 2021. We excluded studies with missing data on humoral or cell-mediated immune response, unspecified methodology of response testing, unspecified timeframes between vaccination and blood sampling or low number of participants (≤3). We excluded individual patients with prior COVID-19 or incomplete vaccine courses. Primary endpoints were humoral and cell-mediated immune response rates. Subgroup analyses included time since anti-CD20 therapy, B cell depletion and indication for anti-CD20 therapy. We used random-effects models of proportions.FindingsNinety studies were assessed. Inclusion criteria were met by 23 studies comprising 1342 patients. Overall rate of humoral response was 0.40 (95% CI 0.35 to 0.47). Overall rate of cell-mediated immune responses was 0.71 (95% CI 0.57 to 0.87). A time interval >6 months since last anti-CD20 therapy was associated with higher humoral response rates with 0.63 (95% CI 0.53 to 0.72) versus <6 months 0.2 (95% CI 0.03 to 0.43); p=0<01. Similarly, patients with circulating B cells more frequently showed humoral responses. Anti-CD20-treated kidney transplant recipients showed lower humoral response rates than patients with haematological malignancies or autoimmune disease.InterpretationPatients on anti-CD20 therapies can develop humoral and cell-mediated immune responses after SARS-CoV-2 vaccination, but subgroups such as kidney transplant recipients or those with very recent therapy and depleted B cell are at high risk for non-seroconversion and should be individually assessed for personalised SARS-CoV-2 vaccination strategies. Potential limitations are small patient numbers and heterogeneity of studies included.FundingThis study was funded by Bern University Hospital.

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22

Pleyer, Christopher, Kerry J. Laing, Mir A. Ali, Christopher L. McClurkan, Susan Soto, Inhye E. Ahn, Pia Nierman, et al. "BTK inhibitors impair humoral and cellular responses to recombinant zoster vaccine in CLL." Blood Advances 6, no. 6 (March 15, 2022): 1732–40. http://dx.doi.org/10.1182/bloodadvances.2021006574.

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Abstract Vaccinations effectively prevent infections; however, patients with chronic lymphocytic leukemia (CLL) have reduced antibody responses following vaccinations. Combined humoral and cellular immune responses to novel adjuvanted vaccines are not well characterized in CLL. In an open-label, single-arm clinical trial, we measured the humoral and cellular immunogenicity of the recombinant zoster vaccine (RZV) in CLL patients who were treatment naïve (TN) or receiving Bruton tyrosine kinase inhibitor (BTKi) therapy. The primary endpoint was antibody response to RZV (≥fourfold increase in anti-glycoprotein E [anti-gE]). Cellular response of gE-specific CD4+ T cells was assessed by flow cytometry for upregulation of ≥2 effector molecules. The antibody response rate was significantly higher in the TN cohort (76.8%; 95% confidence interval [CI], 65.7-87.8) compared with patients receiving a BTKi (40.0%; 95% CI, 26.4-53.6; P = .0002). The cellular response rate was also significantly higher in the TN cohort (70.0%; 95% CI, 57.3-82.7) compared with the BTKi group (41.3%; 95% CI, 27.1-55.5; P = .0072). A concordant positive humoral and cellular immune response was observed in 69.1% (95% CI, 56.9-81.3) of subjects with a humoral response, whereas 39.0% (95% CI, 24.1-54.0) of subjects without a humoral response attained a cellular immune response (P = .0033). Antibody titers and T-cell responses were not correlated with age, absolute B- and T-cell counts, or serum immunoglobulin levels (all P > .05). RZV induced both humoral and cellular immune responses in treated and untreated CLL patients, albeit with lower response rates in patients on BTKi therapy compared with TN patients. This trial was registered at www.clinicaltrials.gov as #NCT03702231.

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23

Toptygina, A. P., T. A. Mamaeva, and V. A. Alioshkin. "PECULIARITIES OF SPECIFIC HUMORAL MESLES IMMUNE RESPONSE." Russian Journal of Infection and Immunity 3, no. 3 (July 7, 2014): 243. http://dx.doi.org/10.15789/2220-7619-2013-3-243-250.

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24

Woo, Patrick C. Y., Hoi-Wah Tsoi, Lei-Po Wong, Harry C. H. Leung, and Kwok-Yung Yuen. "Antibiotics Modulate Vaccine-Induced Humoral Immune Response." Clinical Diagnostic Laboratory Immunology 6, no. 6 (November 1, 1999): 832–37. http://dx.doi.org/10.1128/cdli.6.6.832-837.1999.

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ABSTRACT The effects of antibiotics on the antigen-specific humoral immune response are not known. Macrolides, tetracyclines, and beta-lactams are commonly prescribed antibiotics. The first two are known to have immunomodulatory activities. The effects of clarithromycin, doxycycline, and ampicillin on the primary and secondary antibody responses to tetanus toxoid, a pneumococcal polysaccharide vaccine, a hepatitis B virus surface antigen (HBsAg) vaccine, and live attenuatedSalmonella typhi (Ty21a) were investigated using a mouse model. For the mice receiving the tetanus toxoid, the immunoglobulin M (IgM) level of the clarithromycin group at day 7 was significantly lower than the corresponding antibody level of the normal saline (NS) group. For the mice receiving the pneumococcal polysaccharide vaccine, the total antibody and IgM levels of the clarithromycin group and the IgM level of the doxycycline group at day 7 were significantly lower than the corresponding antibody levels of the ampicillin and NS groups. For the mice receiving the HBsAg vaccine, the IgM level of the doxycycline group at day 7 was significantly lower than the corresponding antibody levels of the clarithromycin and NS groups, while the IgM level of the clarithromycin group at day 28 was significantly lower than the corresponding antibody levels of the doxycycline, ampicillin, and NS groups. For the mice receiving all three vaccines, there were no statistically significant differences between any of the antibody levels of the ampicillin group and the corresponding antibody levels of the NS group. For the mice receiving Ty21a, the total antibody levels of the ampicillin group at days 7 and 21 were significantly higher than the corresponding antibody levels of the NS group. Moreover, the IgM levels of the clarithromycin, doxycycline, and ampicillin groups at days 7 and 21 were significantly higher than the corresponding antibody levels of the NS group. Furthermore, the total antibody level of the ampicillin group at day 21 was significantly higher than the corresponding antibody level of the doxycycline group. For all four vaccines, there were no statistically significant differences among the serum levels of interleukin-10 and gamma interferon for the mice treated with the various antibiotics. We conclude that clarithromycin and doxycycline, but not ampicillin, suppress the antibody responses of mice to T-cell-dependent and T-cell-independent antigens, whereas all three antibiotics enhance the antibody response to live attenuated mucosal bacterial vaccines.

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25

Mosier, D. A., T. L. Kuhls, K. R. Simons, and R. D. Oberst. "Bovine humoral immune response to Cryptosporidium parvum." Journal of Clinical Microbiology 30, no. 12 (1992): 3277–79. http://dx.doi.org/10.1128/jcm.30.12.3277-3279.1992.

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26

Ghione, M., P. A. Clerici, G. Piragine, and E. Magliano. "Humoral circulatory immune response to Gardnerella vaginalis." Journal of Clinical Microbiology 27, no. 9 (1989): 2138–39. http://dx.doi.org/10.1128/jcm.27.9.2138-2139.1989.

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27

Greene, Bruce M. "Cellular and Humoral Immune Response in Onchocerciasis." Journal of Infectious Diseases 165, no. 6 (June 1992): 1161. http://dx.doi.org/10.1093/infdis/165.6.1161b.

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28

Carter, Joseph J., and Denise A. Galloway. "Humoral immune response to human papillomavirus infection." Clinics in Dermatology 15, no. 2 (March 1997): 229–36. http://dx.doi.org/10.1016/s0738-081x(96)00166-6.

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29

Matheson, David S., Bridget J. Green, Marvin J. Fritzler, Man-Chiu Poon, Thomas J. Bowen, and David I. Hoar. "Humoral immune response in patients with hemophilia." Clinical Immunology and Immunopathology 44, no. 1 (July 1987): 41–50. http://dx.doi.org/10.1016/0090-1229(87)90050-x.

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30

Uher, Ferenc, Éva Rajnavölgyi, and Anna Erdei. "Novel regulators of the humoral immune response." Immunology Today 13, no. 8 (January 1992): A4—A6. http://dx.doi.org/10.1016/0167-5699(92)90055-c.

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31

Prellner, Karin, and Olof Kalm. "Humoral Immune Response in Acute Otitis Media." Acta Oto-Laryngologica 105, sup457 (January 1988): 133–38. http://dx.doi.org/10.3109/00016488809138896.

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32

Herroelen, Pauline H., Geert A. Martens, Dieter De Smet, Koen Swaerts, and An-Sofie Decavele. "Humoral Immune Response to SARS-CoV-2." American Journal of Clinical Pathology 154, no. 5 (August 18, 2020): 610–19. http://dx.doi.org/10.1093/ajcp/aqaa140.

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Abstract Objectives Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) serology tests are clinically useful to document prior SARS-CoV-2 infections. Data are urgently needed to select assays with optimal sensitivity at acceptable specificity for antibody detection. Methods A comparative evaluation was performed of 7 commercial SARS-CoV-2 serology assays on 171 sera from 135 subjects with polymerase chain reaction–confirmed SARS-CoV-2 infection (71 hospitalized patients and 64 paucisymptomatic individuals). Kinetics of IgA/IgM/IgG seroconversion to viral N and S protein epitopes were studied from 0 to 54 days after onset of symptoms. Cross-reactivity was verified on 57 prepandemic samples. Results Wantai SARS-COV-2 Ab ELISA and Orient Gene COVID-19 IgG/IgM Rapid Test showed superior overall sensitivity for detection of SARS-CoV-2 antibodies. Elecsys Anti-SARS-CoV-2 assay and EUROIMMUN Anti-SARS-CoV-2 combined IgG/IgA showed acceptable sensitivity (>95%) vs the consensus result of all assays from 10 days post onset of symptoms. Wantai SARS-COV-2 Ab ELISA, Elecsys Anti-SARS-CoV-2 assay, and Innovita 2019-nCoV Ab rapid test showed least cross-reactivity, resulting in an optimal analytical specificity greater than 98%. Conclusions Wantai SARS-COV-2 Ab ELISA and Elecsys Anti-SARS-CoV-2 assays are suitable for sensitive and specific detection of SARS-CoV-2 antibodies from 10 days after onset of symptoms.

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33

Brage, M., A. Holmlund, and A. Johansson. "Humoral immune response to Aggregatibacter actinomycetemcomitans leukotoxin." Journal of Periodontal Research 46, no. 2 (December 1, 2010): 170–75. http://dx.doi.org/10.1111/j.1600-0765.2010.01325.x.

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34

Boothby, Mark, and Robert C. Rickert. "Metabolic Regulation of the Immune Humoral Response." Immunity 46, no. 5 (May 2017): 743–55. http://dx.doi.org/10.1016/j.immuni.2017.04.009.

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35

Van Rooijen, N. "The humoral immune response in the spleen." Research in Immunology 142, no. 4 (January 1991): 328–30. http://dx.doi.org/10.1016/0923-2494(91)90084-v.

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36

Aeumjaturapat, S. "Tonsillectomy และ adenoidectomy กับ humoral immune response." Chulalongkorn Medical Journal 43, no. 7 (July 1999): 501–8. http://dx.doi.org/10.58837/chula.cmj.43.7.6.

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37

John, Lijo, and Rahul Vijay. "Role of TAM Receptors in Antimalarial Humoral Immune Response." Pathogens 13, no. 4 (April 2, 2024): 298. http://dx.doi.org/10.3390/pathogens13040298.

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Immune response against malaria and the clearance of Plasmodium parasite relies on germinal-center-derived B cell responses that are temporally and histologically layered. Despite a well-orchestrated germinal center response, anti-Plasmodium immune response seldom offers sterilizing immunity. Recent studies report that certain pathophysiological features of malaria such as extensive hemolysis, hypoxia as well as the extrafollicular accumulation of short-lived plasmablasts may contribute to this suboptimal immune response. In this review, we summarize some of those studies and attempt to connect certain host intrinsic features in response to the malarial disease and the resultant gaps in the immune response.

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38

Hu, Hui, Xinya Lu, Ling Tao, Bingke Bai, Zhenfeng Zhang, Yao Chen, Fangliang Zheng, Jianjun Chen, Ze Chen, and Hanzhong Wang. "Induction of Specific Immune Responses by Severe Acute Respiratory Syndrome Coronavirus Spike DNA Vaccine with or without Interleukin-2 Immunization Using Different Vaccination Routes in Mice." Clinical and Vaccine Immunology 14, no. 7 (May 9, 2007): 894–901. http://dx.doi.org/10.1128/cvi.00019-07.

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ABSTRACT DNA vaccines induce humoral and cellular immune responses in animal models and humans. To analyze the immunogenicity of the severe acute respiratory syndrome (SARS) coronavirus (CoV), SARS-CoV, spike DNA vaccine and the immunoregulatory activity of interleukin-2 (IL-2), DNA vaccine plasmids pcDNA-S and pcDNA-IL-2 were constructed and inoculated into BALB/c mice with or without pcDNA-IL-2 by using three different immunization routes (the intramuscular route, electroporation, or the oral route with live attenuated Salmonella enterica serovar Typhimurium). The cellular and humoral immune responses were assessed by enzyme-linked immunosorbent assays, lymphocyte proliferation assays, enzyme-linked immunospot assays, and fluorescence-activated cell sorter analyses. The results showed that specific humoral and cellular immunities could be induced in mice by inoculating them with SARS-CoV spike DNA vaccine alone or by coinoculation with IL-2-expressing plasmids. In addition, the immune response levels in the coinoculation groups were significantly higher than those in groups receiving the spike DNA vaccine alone. The comparison between the three vaccination routes indicated that oral vaccination evoked a vigorous T-cell response and a weak response predominantly with subclass immunoglobulin G2a (IgG2a) antibody. However, intramuscular immunization evoked a vigorous antibody response and a weak T-cell response, and vaccination by electroporation evoked a vigorous response with a predominant subclass IgG1 antibody response and a moderate T-cell response. Our findings show that the spike DNA vaccine has good immunogenicity and can induce specific humoral and cellular immunities in BALB/c mice, while IL-2 plays an immunoadjuvant role and enhances the humoral and cellular immune responses. Different vaccination routes also evoke distinct immune responses. This study provides basic information for the design of DNA vaccines against SARS-CoV.

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39

El Moussaoui, Majdouline, Salomé Desmecht, Nicolas Lambert, Nathalie Maes, Joachim Braghini, Nicole Marechal, Céline Quintana, et al. "Cluster Analysis Identifies Distinct Patterns of T-Cell and Humoral Immune Responses Evolution Following a Third Dose of SARS-CoV-2 Vaccine in People Living with HIV." Viruses 15, no. 7 (June 26, 2023): 1435. http://dx.doi.org/10.3390/v15071435.

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(1) Background: Many vaccines require higher, additional doses or adjuvants to provide adequate protection for people living with HIV (PLWH). Despite their potential risk of severe coronavirus disease 2019, immunological data remain sparse, and a clear consensus for the best booster strategy is lacking. (2) Methods: Using the data obtained from our previous study assessing prospective T-cell and humoral immune responses before and after administration of a third dose of SARS-CoV-2 vaccine, we assessed the correlations between immune parameters reflecting humoral and cellular immune responses. We further aimed at identifying distinct clusters of patients with similar patterns of immune response evolution to determine how these relate to demographic and clinical factors. (3) Results: Among 80 PLWH and 51 healthcare workers (HCWs) enrolled in the study, cluster analysis identified four distinct patterns of evolution characterised by specific immune patterns and clinical factors. We observed that immune responses appeared to be less robust in cluster A, whose individuals were mostly PLWH who had never been infected with SARS-CoV-2. Cluster C, whose individuals showed a particularly drastic increase in markers of humoral immune response following the third dose of vaccine, was mainly composed of female participants who experienced SARS-CoV-2. Regarding the correlation study, although we observed a strong positive correlation between markers mirroring humoral immune response, markers of T-cell response following vaccination correlated only in a lesser extent with markers of humoral immunity. This suggests that neutralising antibody titers alone are not always a reliable reflection of the magnitude of the whole immune response. (4) Conclusions: Our findings show heterogeneity in immune responses among SARS-CoV-2 vaccinated PLWH. Specific subgroups could therefore benefit from distinct immunization strategies. Prior or breakthrough natural infection enhances the activity of vaccines and must be taken into account for informing global vaccine strategies among PLWH, even those with a viro-immunologically controlled infection.

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40

La Civita, Evelina, Carla Zannella, Stefano Brusa, Paolo Romano, Elisa Schettino, Fabrizio Salemi, Rosa Carrano, et al. "BNT162b2 Elicited an Efficient Cell-Mediated Response against SARS-CoV-2 in Kidney Transplant Recipients and Common Variable Immunodeficiency Patients." Viruses 15, no. 8 (July 30, 2023): 1659. http://dx.doi.org/10.3390/v15081659.

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SARS-CoV-2 vaccination is the standard of care for the prevention of COVID-19 disease. Although vaccination triggers both humoral and cellular immune response, COVID-19 vaccination efficacy is currently evaluated by measuring antibodies only, whereas adaptative cellular immunity is unexplored. Our aim is to test humoral and cell-mediated response after three doses of BNT162b vaccine in two cohorts of fragile patients: Common Variable Immunodeficiency (CVID) patients and Kidney Transplant Recipients (KTR) patients compared to healthy donors. We enrolled 10 healthy controls (HCs), 19 CVID patients and 17 KTR patients. HC BNT162b third dose had successfully mounted humoral immune response. A positive correlation between Anti-Spike Trimeric IgG concentration and neutralizing antibody titer was also observed. CVID and KTR groups showed a lower humoral immune response compared to HCs. IFN-γ release induced by epitopes of the Spike protein in stimulated CD4+ and CD8+ T cells was similar among vaccinated HC, CVID and KTR. Patients vaccinated and infected showed a more efficient humoral and cell-mediated response compared to only vaccinated patients. In conclusion, CVID and KTR patients had an efficient cell-mediated but not humoral response to SARS-CoV-2 vaccine, suggesting that the evaluation of T cell responses could be a more sensitive marker of immunization in these subjects.

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41

Kong, Wing-pui, Ling Xu, Konrad Stadler, Jeffrey B. Ulmer, Sergio Abrignani, Rino Rappuoli, and Gary J. Nabel. "Modulation of the Immune Response to the Severe Acute Respiratory Syndrome Spike Glycoprotein by Gene-Based and Inactivated Virus Immunization." Journal of Virology 79, no. 22 (November 15, 2005): 13915–23. http://dx.doi.org/10.1128/jvi.79.22.13915-13923.2005.

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ABSTRACT Although the initial isolates of the severe acute respiratory syndrome (SARS) coronavirus (CoV) are sensitive to neutralization by antibodies through their spike (S) glycoprotein, variants of S have since been identified that are resistant to such inhibition. Optimal vaccine strategies would therefore make use of additional determinants of immune recognition, either through cellular or expanded, cross-reactive humoral immunity. Here, the cellular and humoral immune responses elicited by different combinations of gene-based and inactivated viral particles with various adjuvants have been assessed. The T-cell response was altered by different prime-boost immunizations, with the optimal CD8 immunity induced by DNA priming and replication-defective adenoviral vector boosting. The humoral immune response was enhanced most effectively through the use of inactivated virus with adjuvants, either MF59 or alum, and was associated with stimulation of the CD4 but not the CD8 response. The use of inactivated SARS virus with MF59 enhanced the CD4 and antibody response even after gene-based vaccination. Because both cellular and humoral immune responses are generated by gene-based vaccination and inactivated viral boosting, this strategy may prove useful in the generation of SARS-CoV vaccines.

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Fedorov, Vyacheslav S., Olga N. Ivanova, Inna L. Karpenko, and Alexander V. Ivanov. "The immune response to the novel coronavirus infection." Journal of Clinical Practice 12, no. 1 (May 7, 2021): 33–40. http://dx.doi.org/10.17816/clinpract64677.

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This review summarizes the current knowledge on the humoral and T-cell immunity to the novel coronavirus infection. A special attention is paid to the viral proteins that induce production of antibodies, different types of immunoglobulins and their role in the protection against the virus as well as to the duration of the humoral immune response. In addition, a concise analysis of the T-cell immunity status during COVID-19 and its input into the antiviral defense is presented. The collected data demonstrating preservation of both the humoral and T-cell immunity are urgently needed in the medical professionals' community for evidence-based decisions on the immunity monitoring, estimation of (re)vaccination time, as well as for knowing the factors that should be considered while choosing the most effective vaccine. Finally, several directions for the future research are pointed out

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Rosseto-Welter, Eliane Aparecida, Silvia Sanches Rodrigues, Amanda Braga de Figueiredo, Carolina Nunes França, Danielle Bruna Leal Oliveira, André Luis Lacerda Bachi, Jônatas Bussador do Amaral, et al. "Cellular and Humoral Immune Responses to Vaccination for COVID-19 Are Negatively Impacted by Senescent T Cells: A Case Report." Vaccines 11, no. 4 (April 14, 2023): 840. http://dx.doi.org/10.3390/vaccines11040840.

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Background: Herein, we aimed to follow up on the cellular and humoral immune responses of a group of individuals who initially received the CoronaVac vaccine, followed by a booster with the Pfizer vaccine. Methods: Blood samples were collected: before and 30 days after the first CoronaVac dose; 30, 90, and 180 days after the second CoronaVac dose, and also 20 days after the booster with the Pfizer vaccine. Results: Whilst the positivity to gamma interferon-type cellular response increased after the first CoronaVac dose, neutralizing and IgG antibody levels only raised 30 days after the second dose, followed by a drop in these responses after 90 and 180 days. The booster with the Pfizer vaccine elicited a robust cellular and humoral response. A higher number of double-negative and senescent T cells, as well as increased pro-inflammatory cytokines levels were found in the participants with lower humoral immune responses. Conclusion: CoronaVac elicited an early cellular response, followed by a humoral response, which dropped 90 days after the second dose. The booster with the Pfizer vaccine significantly enhanced these responses. Furthermore, a pro-inflammatory systemic status was found in volunteers who presented senescent T cells, which could putatively impair the immune response to vaccination.

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Michael John Dochniak. "Allergies, acute infections and humoral skin creams." International Journal of Biology and Pharmacy Research Updates 2, no. 1 (September 30, 2022): 014–16. http://dx.doi.org/10.53430/ijbpru.2022.2.1.0033.

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Allergies can engender a healthy immune response to harmful viruses. The humoral immune system (i.e., antibody-mediated immunity) creates and regulates endogenous proteins that support a fully integrated immune response to acute infections. A robust and active humoral immune system may inhibit the development of cytokine/bradykinin storms and affect angiotensin-converting enzyme 2 (ACE2) expression. Humoral skin cream therapy is immune-stimulating and may affect the global burden of morbidity and mortality from acute infections.

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Cerón-Gómez, Miller, and Hyun Mo Yang. "Global dynamics of humoral and cellular immune responses to virus infection." Universitas Scientiarum 24, no. 2 (August 8, 2019): 407–23. http://dx.doi.org/10.11144/javeriana.sc24-2.gdoh.

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We study the global stability of a model of virus dynamics with consideration of humoral and cellular immune responses. We use a Lyapunov direct method to obtain sufficient conditions for the global stability of virus free and viruspresence equilibriums. First, we analyze the model without an immune response and found that if the reproductive number of the virus is less than or equal to one, the virus-free equilibrium is globally asymptotically stable. However, for the virus-presence equilibrium, global stability is obtained if the virus entrance rate into the target cells is less than one. We analyze the model with humoral and cellular immune responses and found similar results. The difference is that in the reproductive number of the virus and in the virus entrance rate into the target cells appear parameters of humoral and cellular immune responses, which means that the adaptive immune response will cease or control the rise of the infection.

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Hocknell, Peter K., Rebecca D. Wiley, Xiuqing Wang, Thomas G. Evans, William J. Bowers, Tomas Hanke, Howard J. Federoff, and Stephen Dewhurst. "Expression of Human Immunodeficiency Virus Type 1 gp120 from Herpes Simplex Virus Type 1-Derived Amplicons Results in Potent, Specific, and Durable Cellular and Humoral Immune Responses." Journal of Virology 76, no. 11 (June 1, 2002): 5565–80. http://dx.doi.org/10.1128/jvi.76.11.5565-5580.2002.

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ABSTRACT Herpes simplex virus type 1 (HSV-1) infects a wide range of cells, including dendritic cells. Consequently, HSV-1 vectors may be capable of eliciting strong immune responses to vectored antigens. To test this hypothesis, an HSV-1 amplicon plasmid encoding human immunodeficiency virus type 1 gp120 was constructed, and murine immune responses to helper virus-free amplicon preparations derived from this construct were evaluated. Initial studies revealed that a single intramuscular (i.m.) injection of 106 infectious units (i.u.) of HSV:gp120 amplicon particles (HSV:gp120) elicited Env-specific cellular and humoral immune responses. A potent, CD8+-T-cell-mediated response to an H-2Dd-restricted peptide from gp120 (RGPGRAFVTI) was measured by a gamma interferon ELISPOT and was confirmed by standard cytotoxic-T-lymphocyte assays. Immunoglobulin G enzyme-linked immunosorbent assay analysis showed the induction of a strong, Env-specific antibody response. An i.m. or an intradermal administration of HSV:gp120 at the tail base elicited a more potent cellular immune response than did an intraperitoneal (i.p.) inoculation, although an i.p. introduction generated a stronger humoral response. The immune response to HSV:gp120 was durable, with robust cellular and humoral responses persisting at 171 days after a single 106-i.u. inoculation. The immune response to HSV:gp120 was also found to be dose dependent: as few as 104 i.u. elicited a strong T-cell response. Finally, HSV:gp120 elicited significant Env-specific cellular immune responses even in animals that had been previously infected with wild-type HSV-1. Taken together, these data strongly support the use of helper-free HSV-1 amplicon particles as vaccine delivery vectors.

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Zhang, Jingyao, Wenjuan Gao, Qirui Guo, Bobo Huang, Bin Wang, Guoliang Xia, and Youmin Kang. "Helminth Protein Vaccine Induced Follicular T Helper Cell for Enhancement of Humoral Immunity againstSchistosoma japonicum." BioMed Research International 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/798164.

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Protein vaccines combined with adjuvants have been widely used to induce immune responses, especially the humoral immune response, against molecular targets including parasites. Follicular T helper (Tfh) cells are the specialized providers of B-cell help, however, the induction of Tfh cells in protein vaccination has been rarely studied. Here, we report that theSchistosoma japonicumrecombinant protein (SjGST-32) combined with tacrolimus (FK506) augmented the induction of Tfh cells, which expressed the canonical markers CXCR5, BCL6, and IL-21, and enhanced the humoral immune responses in BALB/c mice. Furthermore, the expression of IL-21R on germinal center (GC) B cells and memory B cells increased in immunized mice, which indicated that IL-21 from the induced Tfh cells interacted with IL-21R for activation of B cells and maintenance of long-lived humoral immunity. Our results suggest that helminth protein vaccine combined with FK506 induces Tfh cell for stimulating humoral immune responses and inducing long-lived humoral immunity.

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Suzue, K., and R. A. Young. "Adjuvant-free hsp70 fusion protein system elicits humoral and cellular immune responses to HIV-1 p24." Journal of Immunology 156, no. 2 (January 15, 1996): 873–79. http://dx.doi.org/10.4049/jimmunol.156.2.873.

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Abstract Heat shock proteins are major targets of the immune response to bacterial and parasitic pathogens. Mycobacterium tuberculosis hsp70 is an especially powerful Ag containing multiple B and T cell epitopes. We investigated whether M. tuberculosis hsp70 can be used as an adjuvant-free carrier to stimulate the humoral and cellular immune response to an accompanying protein. A recombinant hsp70 protein expression vector was developed that permits the production of any protein fused to the amino terminus of mycobacterial hsp70. We found that a recombinant HIV p24-hsp70 fusion protein produced with this vector elicited both humoral and cellular immune responses against p24 in mice when administered in saline in the absence of adjuvant. Covalent linkage of hsp70 to p24 was essential to elicit immune responses to p24 under these conditions. The anti-p24 IgG1 Abs induced in p24-hsp70-immunized mice persisted at high levels for more than 1 yr after immunization. These results demonstrate that the antigenic properties of M. tuberculosis hsp70 can be exploited to enhance the humoral and cellular immune response to an attached protein.

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Weng, Wen-Kai, Debra Czerwinski, and Ronald Levy. "Humoral Immune Response and Immunoglobulin G Fc Receptor Genotype Are Associated with Better Clinical Outcome Following Idiotype Vaccination in Follicular Lymphoma Patients Regardless of Their Response to Induction Chemotherapy." Blood 106, no. 11 (November 16, 2005): 777. http://dx.doi.org/10.1182/blood.v106.11.777.777.

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Abstract Recently, we found that anti-idiotype humoral immune response and FcγRIIIa 158 Valine/Valine (V/V) correlated with clinical outcome in follicular lymphoma patients receiving idiotype vaccination (JCO 22:4717). This result highlighted the importance of developing anti-tumor antibodies and hosting an efficient ADCC machinery. In the previous study, all 136 patients received induction chemotherapy and were in clinical remission at the time of idiotype vaccination. One important question is whether the outcome of these patients was correlated with their clinical response to induction chemotherapy. We, therefore, analyzed the impact of chemotherapy response on clinical outcome to determine if the better outcome associated with humoral immune response and V/V genotype applies to patients with different chemotherapy response. Induction cheomtherapies included chlorambucil, CVP, an adriamycin-containing regimen, or alternating CVP and fludarabine. Ninety patients (66%) achieved complete response or unconfirmed complete response (CR/CRu) and 46 patient (34%) achieved partial response (PR). The progression free survival at 4 years was 59% for CR/CRu patients and 41% for PR patients. The median time to progression (TTP) of 5.21 for CR/CRu patients was significantly longer than the 1.62 years for PR patients (p=0.004). Multi-variant analysis using the Cox Proportional Hazards Model showed that humoral IR, V/V genotype and CR/CRu were three independent positive predictors for progression free survival, while FcγRIIa genotype, FcγRIIb genotype, cellular IR, gender, age, B symptoms, time from diagnosis to therapy, use of adriamycin or use of fludarabine during induction chemotherapy had no impact. The relative benefit was 2.26 (95% CI, 1.36–3.76, p=0.0016) for humoral IR, 5.03 (95% CI, 2.06–12.25, p=0.0004) for V/V genotype and 2.01 (95% CI, 1.22–3.29, p=0.0057) for CR/CRu. The impact of humoral immune response and V/V genotype on CR/CRu or PR patients were then examined. In CR/CRu patients, the progression free survival at 4 years was 74% for patients with humoral immune response and/or V/V genotype while only 45% for patients without either, with median TTP not reached and of 3.46 years for the two groups, respectively (p=0.007). In PR patients, the benefit of having humoral immune response and/or V/V genotype was even more pronounced. The progression free survival at 4 years was 63% for patients with humoral immune response and/or V/V genotype and 21% for patients without either, with median TTP not reached after 8 years and of 1.31 years for the two groups, respectively (p=0.0004). This result suggests that having humoral immune response and/or V/V genotype was associated with longer TTP regardless of their response to induction chemotherapy. In fact, there is no difference in the TTP between CR/CRu and PR patients if they had humoral immune response and/or V/V genotype (TTP not reached in both groups, p=0.338). In contrast, in the group with neither humoral immune response nor V/V genotype, CR/CRu patients enjoyed much longer TTP than PR patients (TTP 3.46 year vs 1.31 years, p=0.0005). This result further confirms the strong association of clinical outcome with humoral immune response and with the functional activity of Fc receptor bearing cells in patients receiving idiotype vaccination. Our results also argue for the inclusion of PR as well as CR patients in idiotype vaccine trials, since the apparent benefit of immune response is even greater in PR patients.

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Abravanel, Florence, Olivier Marion, Arnaud Del Bello, Thomas Beunon, Raphaelle Romieu-Mourez, Chloé Couat, Mélanie Pucelle, et al. "Humoral and Cellular Immune Responses of Solid Organ Transplant Patients on Belatacept to Three Doses of mRNA-Based Anti-SARS-CoV-2 Vaccine." Vaccines 10, no. 3 (February 24, 2022): 354. http://dx.doi.org/10.3390/vaccines10030354.

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Background: Two doses of anti-SARS-CoV-2 mRNA-based vaccines are poorly immunogenic in solid organ transplant recipients (SOT). Methods: In total, 68 belatacept-treated SOT recipients followed at the Toulouse University Hospital were investigated. They were given three injections of the BNT162b2 mRNA COVID-19 vaccine. Their humoral response was assessed by determining anti-spike antibodies and neutralizing antibodies. The T-cell responses were assessed using an enzyme-linked immunospot assay that measured the interferon-γ produced by specific SARS-CoV-2 T-cells in a subgroup of 17 patients. Results: Only 23.5% of these patients developed a detectable anti-spike response. Moreover, the cellular and the humoral responses were well correlated. Patients with no humoral response were also without a detectable cellular response. Those belatacept-treated patients who developed an Anti-SARS-CoV-2 humoral response were younger, had been transplanted for longer, and had a higher lymphocyte count and a better glomerular filtration rate than those with no response. Finally, patients on tacrolimus plus belatacept produced a lower immune response. Conclusions: Belatacept-treated SOT recipients have a reduced immune response to anti-SARS-CoV-2 mRNA vaccination. The vaccine should be given quite separately from the belatacept infusion to improve immunogenicity. Studies to assess whether switching to another immunosuppressive regimen can improve the post-vaccination immune response would be useful.

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