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Bibliografías temáticas / Protective Immunity / Artículos de revistas

Artículos de revistas sobre el tema "Protective Immunity"

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Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 20 de febrero de 2023

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1

Burger, Eva. "Paracoccidioidomycosis Protective Immunity". Journal of Fungi 7, n.º 2 (13 de febrero de 2021): 137. http://dx.doi.org/10.3390/jof7020137.

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Protective immunity against Paracoccidioides consists of a stepwise activation of numerous effector mechanisms that comprise many cellular and soluble components. At the initial phase of non-specific innate immunity, resistance against Paracoccidioides comes from phagocytic polymorphonuclear neutrophils, natural killer (NK) cells and monocytes, supplemented by soluble factors such as cytokines and complement system components. Invariant receptors (Toll-like receptors (TLRs), Dectins) which are present in cells of the immune system, detect patterns present in Paracoccidioides (but not in the host) informing the hosts cells that there is an infection in progress, and that the acquired immunity must be activated. The role of components involved in the innate immunity of paracoccidioidomycosis is herein presented. Humoral immunity, represented by specific antibodies which control the fungi in the blood and body fluids, and its role in paracoccidioidomycosis (which was previously considered controversial) is also discussed. The protective mechanisms (involving various components) of cellular immunity are also discussed, covering topics such as: lysis by activated macrophages and cytotoxic T lymphocytes, the participation of lytic products, and the role of cytokines secreted by T helper lymphocytes in increasing the efficiency of Paracoccidioides, lysis.

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2

Hoerauf, Achim y Cathy Steel. "3.2 PROTECTIVE IMMUNITY—VACCINES". American Journal of Tropical Medicine and Hygiene 71, n.º 5_suppl (1 de noviembre de 2004): 34–36. http://dx.doi.org/10.4269/ajtmh.2004.71.5_suppl.0700034.

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3

Cox, R. A. y D. M. Magee. "Protective immunity in coccidioidomycosis". Research in Immunology 149, n.º 4-5 (mayo de 1998): 417–28. http://dx.doi.org/10.1016/s0923-2494(98)80765-7.

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4

Huang, Shou-Jie, Xiao-Hui Liu, Jun Zhang y Mun-Hon Ng. "Protective immunity against HEV". Current Opinion in Virology 5 (abril de 2014): 1–6. http://dx.doi.org/10.1016/j.coviro.2013.10.003.

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5

Zinkernagel, Rolf M. "Immunological memory ≠ protective immunity". Cellular and Molecular Life Sciences 69, n.º 10 (6 de abril de 2012): 1635–40. http://dx.doi.org/10.1007/s00018-012-0972-y.

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6

Lin, Wen-Hsuan y Diane E. Griffin. "138 Understanding protective immunity". JAIDS Journal of Acquired Immune Deficiency Syndromes 65 (abril de 2014): 58. http://dx.doi.org/10.1097/01.qai.0000446718.70725.4b.

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7

Watson, J. D. "Leprosy: understanding protective immunity". Immunology Today 10, n.º 7 (julio de 1989): 218–21. http://dx.doi.org/10.1016/0167-5699(89)90253-3.

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8

Watanabe, Mineo y Masaaki Nagai. "Role of Systemic and Mucosal Immune Responses in Reciprocal Protection against Bordetella pertussis and Bordetella parapertussis in a Murine Model of Respiratory Infection". Infection and Immunity 71, n.º 2 (febrero de 2003): 733–38. http://dx.doi.org/10.1128/iai.71.2.733-738.2003.

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ABSTRACT The roles of systemic humoral immunity, cell-mediated immunity, and mucosal immunity in reciprocal protective immunity against Bordetella pertussis and Bordetella parapertussis were examined by using a murine model of respiratory infection. Passive immunization with serum from mice infected with B. pertussis established protective immunity against B. pertussis but not against B. parapertussis. Protection against B. parapertussis was induced in mice that had been injected with serum from mice infected with B. parapertussis but not from mice infected with B. pertussis. Adoptive transfer of spleen cells from mice infected with B. pertussis or B. parapertussis also failed to confer reciprocal protection. To examine the role of mucosal immunity in reciprocal protection, mice were infected with preparations of either B. pertussis or B. parapertussis, each of which had been incubated with the bronchoalveolar wash of mice that were convalescing after infection with B. pertussis or B. parapertussis. Such incubation conferred reciprocal protection against B. pertussis and B. parapertussis on infected mice. The data suggest that mucosal immunity including secreted immunoglobulin A in the lungs might play an important role in reciprocal protective immunity in this murine model of respiratory infection.

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9

Mokaya, Jolynne, Derick Kimathi, Teresa Lambe y George M. Warimwe. "What Constitutes Protective Immunity Following Yellow Fever Vaccination?" Vaccines 9, n.º 6 (18 de junio de 2021): 671. http://dx.doi.org/10.3390/vaccines9060671.

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Yellow fever (YF) remains a threat to global health, with an increasing number of major outbreaks in the tropical areas of the world over the recent past. In light of this, the Eliminate Yellow Fever Epidemics Strategy was established with the aim of protecting one billion people at risk of YF through vaccination by the year 2026. The current YF vaccine gives excellent protection, but its use is limited by shortages in supply due to the difficulties in producing the vaccine. There are good grounds for believing that alternative fractional dosing regimens can produce strong protection and overcome the problem of supply shortages as less vaccine is required per person. However, immune responses to these vaccination approaches are yet to be fully understood. In addition, published data on immune responses following YF vaccination have mostly quantified neutralising antibody titers. However, vaccine-induced antibodies can confer immunity through other antibody effector functions beyond neutralisation, and an effective vaccine is also likely to induce strong and persistent memory T cell responses. This review highlights the gaps in knowledge in the characterisation of YF vaccine-induced protective immunity in the absence or presence of neutralising antibodies. The assessment of biophysical antibody characteristics and cell-mediated immunity following YF vaccination could help provide a comprehensive landscape of YF vaccine-induced immunity and a better understanding of correlates of protective immunity.

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10

Stingl, G. "PL04.3 Protective and Non-Protective Immunity in STIs". Sexually Transmitted Infections 89, Suppl 1 (julio de 2013): A4.3—A4. http://dx.doi.org/10.1136/sextrans-2013-051184.0011.

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11

Blutt, Sarah E., Kelly L. Warfield, Mary K. Estes y Margaret E. Conner. "Differential Requirements for T Cells in Viruslike Particle- and Rotavirus-Induced Protective Immunity". Journal of Virology 82, n.º 6 (9 de enero de 2008): 3135–38. http://dx.doi.org/10.1128/jvi.01727-07.

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ABSTRACT Correlates of protection from rotavirus infection are controversial. We compared the roles of B and T lymphocytes in protective immunity induced either by intranasally administered nonreplicating viruslike particles or inactivated virus or by orally administered murine rotavirus. We found that protection induced by nonreplicating vaccines requires CD4+ T cells and CD40/CD40L. In contrast, T cells were not required for short-term protective immunity induced by infection, but both T-cell-dependent and -independent mechanisms contributed to long-term maintenance of protection. Our findings indicate that more than one marker of protective immunity exists and that these markers depend on the vaccine that is administered.

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12

Doolan, Denise L. y Stephen L. Hoffman. "Pre–erythrocytic–stage immune effector mechanisms in Plasmodium spp. infections". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, n.º 1359 (29 de septiembre de 1997): 1361–67. http://dx.doi.org/10.1098/rstb.1997.0121.

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The potent protective immunity against malaria induced by immunization of mice and humans with radiation–attenuated Plasmodium spp. sporozoites is thought to be mediated primarily by T–cell responses directed against infected hepatocytes. This has led to considerable efforts to develop subunit vaccines that duplicate this protective immunity, but a universally effective vaccine is still not available and in vitro correlates of protective immunity have not been established. Contributing to this delay has been a lack of understanding of the mechanisms responsible for the protection. There are now data indicating that CD8+ T cells, CD4+ T cells, cytokines, and nitric oxide can all mediate the elimination of infected hepatocytes in vitro and in vivo . By dissecting the protection induced by immunization with irradiated sporozoite, DNA and synthetic peptide–adjuvant vaccines, we have demonstrated that different T–cell–dependent immune responses mediate protective immunity in the same inbred strain of mouse, depending on the method of immunization. Furthermore, the mechanism of protection induced by a single method of immunization may vary among different strains of mice. These data have important implications for the development of pre–erythrocytic–stage vaccines designed to protect a heterogeneous human population, and of assays that predict protective immunity.

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13

Roy, Sreeja, Clare M. Williams, Julian Pardo, Danushka K. Wijesundara y Yoichi Furuya. "Impact of Pre-Existing Immunity on Live Attenuated Influenza Vaccine-Induced Cross-Protective Immunity". Vaccines 8, n.º 3 (20 de agosto de 2020): 459. http://dx.doi.org/10.3390/vaccines8030459.

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The efficacy of the intranasally (i.n.) delivered live attenuated influenza vaccine (LAIV) is variable and, in some seasons, suboptimal. In this study, we report that LAIV exhibits cross-protective efficacy in mice, potentially associated with cellular immunity as opposed to antigen-specific antibody responses. However, pre-exposure to the intramuscularly (i.m.) delivered inactivated influenza vaccine (IIV) severely impaired LAIV-induced cross-protection against heterologous challenge, potentially by inhibiting replication of LAIV. Our findings suggest that pre-existing immunity afforded by IIV suppresses cross-protective T cell immunogenicity of LAIV.

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14

Igarashi, Ikuo, Reiko Suzuki, Seiji Waki, Yoh-Ichi Tagawa, Seyha Seng, Sothyra Tum, Yoshitaka Omata et al. "Roles of CD4+ T Cells and Gamma Interferon in Protective Immunity against Babesia microtiInfection in Mice". Infection and Immunity 67, n.º 8 (1 de agosto de 1999): 4143–48. http://dx.doi.org/10.1128/iai.67.8.4143-4148.1999.

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ABSTRACT Babesia microti produces a self-limiting infection in mice, and recovered mice are resistant to reinfection. In the present study, the role of T cells in protective immunity against challenge infection was examined. BALB/c mice which recovered from primary infection showed strong protective immunity against challenge infection. In contrast, nude mice which failed to control the primary infection and were cured with an antibabesial drug did not show protection against challenge infection. Treatment of immune mice with anti-CD4 monoclonal antibody (MAb) diminished the protective immunity against challenge infection, but treatment with anti-CD8 MAb had no effect on the protection. Transfer of CD4+ T-cell-depleted spleen cells resulted in higher parasitemia than transfer of CD8+ T-cell-depleted spleen cells. A high level of gamma interferon (IFN-γ), which was produced by CD4+ T cells, was observed for the culture supernatant of spleen cells from immune mice, and treatment of immune mice with anti-IFN-γ MAb partially reduced the protection. Moreover, no protection against challenge infection was found in IFN-γ-deficient mice. On the other hand, treatment of immune mice with MAbs against interleukin-2 (IL-2), IL-4, or tumor necrosis factor alpha did not affect protective immunity. These results suggest essential requirements for CD4+ T cells and IFN-γ in protective immunity against challenge infection with B. microti.

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15

Goldman, Gustavo H., Yves Delneste y Nicolas Papon. "Fungal Polysaccharides Promote Protective Immunity". Trends in Microbiology 29, n.º 5 (mayo de 2021): 379–81. http://dx.doi.org/10.1016/j.tim.2021.02.004.

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16

Parodi, Cecilia, Angel Marcelo Padilla y Miguel Angel Basombrío. "Protective immunity against Trypanosoma cruzi". Memórias do Instituto Oswaldo Cruz 104, suppl 1 (julio de 2009): 288–94. http://dx.doi.org/10.1590/s0074-02762009000900038.

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17

Mulupuri, Prasad, Tania Gourley, Adam Popkowski, Aneesh Mehta, Beth Begley, Cynthia Breeden, Christian Larsen y Rafi Ahmed. "Protective Immunity in Transplant Recipients". FASEB Journal 22, S2 (abril de 2008): 532. http://dx.doi.org/10.1096/fasebj.22.2_supplement.532.

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18

ROSS, A. CATHARINE. "Vitamin A and Protective Immunity". Nutrition Today 27, n.º 4 (julio de 1992): 18–26. http://dx.doi.org/10.1097/00017285-199207000-00005.

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19

Lee, Chi-Jen, Lucia H. Lee y Carl E. Frasch. "Protective Immunity of Pneumococcal Glycoconjugates". Critical Reviews in Microbiology 29, n.º 4 (enero de 2003): 333–49. http://dx.doi.org/10.1080/713608018.

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20

Bachmann, Martin F. y Manfred Kopf. "Balancing protective immunity and immunopathology". Current Opinion in Immunology 14, n.º 4 (agosto de 2002): 413–19. http://dx.doi.org/10.1016/s0952-7915(02)00363-1.

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21

Huster, Katharina M., Christian Stemberger y Dirk H. Busch. "Protective immunity towards intracellular pathogens". Current Opinion in Immunology 18, n.º 4 (agosto de 2006): 458–64. http://dx.doi.org/10.1016/j.coi.2006.05.008.

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22

Kapil, Parul y Tod J. Merkel. "Pertussis vaccines and protective immunity". Current Opinion in Immunology 59 (agosto de 2019): 72–78. http://dx.doi.org/10.1016/j.coi.2019.03.006.

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23

Nutman, Thomas B. "Protective immunity in lymphatic filariasis". Experimental Parasitology 68, n.º 2 (febrero de 1989): 248–52. http://dx.doi.org/10.1016/0014-4894(89)90106-9.

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24

Hewitt, Eric W. y Gillian E. Dugan. "Virus subversion of protective immunity". Current Allergy and Asthma Reports 4, n.º 5 (septiembre de 2004): 365–70. http://dx.doi.org/10.1007/s11882-004-0085-2.

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25

Dranoff, Glenn. "Targets of Protective Tumor Immunity". Annals of the New York Academy of Sciences 1174, n.º 1 (septiembre de 2009): 74–80. http://dx.doi.org/10.1111/j.1749-6632.2009.04938.x.

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26

Nilsson, Jan. "Regulating Protective Immunity in Atherosclerosis". Circulation Research 96, n.º 4 (4 de marzo de 2005): 395–97. http://dx.doi.org/10.1161/01.res.0000159183.88730.79.

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27

Fikrig, E., F. S. Kantor, S. W. Barthold y R. A. Flavell. "Protective immunity in lyme borreliosis". Parasitology Today 9, n.º 4 (abril de 1993): 129–31. http://dx.doi.org/10.1016/0169-4758(93)90176-g.

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28

Raeven, René H. M., Naomi van Vlies, Merijn L. M. Salverda, Larissa van der Maas, Joost P. Uittenbogaard, Tim H. E. Bindels, Jolanda Rigters et al. "The Role of Virulence Proteins in Protection Conferred by Bordetella pertussis Outer Membrane Vesicle Vaccines". Vaccines 8, n.º 3 (30 de julio de 2020): 429. http://dx.doi.org/10.3390/vaccines8030429.

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The limited protective immunity induced by acellular pertussis vaccines demands development of novel vaccines that induce broader and longer-lived immunity. In this study, we investigated the protective capacity of outer membrane vesicle pertussis vaccines (omvPV) with different antigenic composition in mice to gain insight into which antigens contribute to protection. We showed that total depletion of virulence factors (bvg(-) mode) in omvPV led to diminished protection despite the presence of high antibody levels. Antibody profiling revealed overlap in humoral responses induced by vaccines in bvg(-) and bvg(+) mode, but the potentially protective responses in the bvg(+) vaccine were mainly directed against virulence-associated outer membrane proteins (virOMPs) such as BrkA and Vag8. However, deletion of either BrkA or Vag8 in our outer membrane vesicle vaccines did not affect the level of protection. In addition, the vaccine-induced immunity profile, which encompasses broad antibody and mixed T-helper 1, 2 and 17 responses, was not changed. We conclude that the presence of multiple virOMPs in omvPV is crucial for protection against Bordetella pertussis. This protective immunity does not depend on individual proteins, as their absence or low abundance can be compensated for by other virOMPs.

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29

Montgomery, Christopher P., Melvin Daniels, Fan Zhao, Maria-Luisa Alegre, Anita S. Chong y Robert S. Daum. "Protective Immunity against Recurrent Staphylococcus aureus Skin Infection Requires Antibody and Interleukin-17A". Infection and Immunity 82, n.º 5 (10 de marzo de 2014): 2125–34. http://dx.doi.org/10.1128/iai.01491-14.

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ABSTRACTAlthough many microbial infections elicit an adaptive immune response that can protect against reinfection, it is generally thought thatStaphylococcus aureusinfections fail to generate protective immunity despite detectable T and B cell responses. No vaccine is yet proven to preventS. aureusinfections in humans, and efforts to develop one have been hampered by a lack of animal models in which protective immunity occurs. Our results describe a novel mouse model of protective immunity against recurrent infection, in whichS. aureusskin and soft tissue infection (SSTI) strongly protected against secondary SSTI in BALB/c mice but much less so in C57BL/6 mice. This protection was dependent on antibody, because adoptive transfer of immune BALB/c serum or purified antibody into either BALB/c or C57BL/6 mice resulted in smaller skin lesions. We also identified an antibody-independent mechanism, because B cell-deficient mice were partially protected against secondaryS. aureusSSTI and adoptive transfer of T cells from immune BALB/c mice resulted in smaller lesions upon primary infection. Furthermore, neutralization of interleukin-17A (IL-17A) abolished T cell-mediated protection in BALB/c mice, whereas neutralization of gamma interferon (IFN-γ) enhanced protection in C57BL/6 mice. Therefore, protective immunity against recurrentS. aureusSSTI was advanced by antibody and the Th17/IL-17A pathway and prevented by the Th1/IFN-γ pathway, suggesting that targeting both cell-mediated and humoral immunity might optimally protect against secondaryS. aureusSSTI. These findings also highlight the importance of the mouse genetic background in the development of protective immunity againstS. aureusSSTI.

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30

Harvill, Eric T., Manuel Osorio, Crystal L. Loving, Gloria M. Lee, Vanessa K. Kelly y Tod J. Merkel. "Anamnestic Protective Immunity to Bacillus anthracis Is Antibody Mediated but Independent of Complement and Fc Receptors". Infection and Immunity 76, n.º 5 (3 de marzo de 2008): 2177–82. http://dx.doi.org/10.1128/iai.00647-07.

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ABSTRACT The threat of bioterrorist use of Bacillus anthracis has focused urgent attention on the efficacy and mechanisms of protective immunity induced by available vaccines. However, the mechanisms of infection-induced immunity have been less well studied and defined. We used a combination of complement depletion along with immunodeficient mice and adoptive transfer approaches to determine the mechanisms of infection-induced protective immunity to B. anthracis. B- or T-cell-deficient mice lacked the complete anamnestic protection observed in immunocompetent mice. In addition, T-cell-deficient mice generated poor antibody titers but were protected by the adoptive transfer of serum from B. anthracis-challenged mice. Adoptively transferred sera were protective in mice lacking complement, Fc receptors, or both, suggesting that they operate independent of these effectors. Together, these results indicate that antibody-mediated neutralization provides significant protection in B. anthracis infection-induced immunity.

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31

Silva, Ediane B., Andrew Goodyear, Marjorie D. Sutherland, Nicole L. Podnecky, Mercedes Gonzalez-Juarrero, Herbert P. Schweizer y Steven W. Dow. "Correlates of Immune Protection following Cutaneous Immunization with an Attenuated Burkholderia pseudomallei Vaccine". Infection and Immunity 81, n.º 12 (7 de octubre de 2013): 4626–34. http://dx.doi.org/10.1128/iai.00915-13.

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ABSTRACTInfections with the Gram-negative bacteriumBurkholderia pseudomallei(melioidosis) are associated with high mortality, and there is currently no approved vaccine to prevent the development of melioidosis in humans. Infected patients also do not develop protective immunity to reinfection, and some individuals will develop chronic, subclinical infections withB. pseudomallei. At present, our understanding of what constitutes effective protective immunity againstB. pseudomalleiinfection remains incomplete. Therefore, we conducted a study to elucidate immune correlates of vaccine-induced protective immunity against acuteB. pseudomalleiinfection. BALB/c and C57BL/6 mice were immunized subcutaneously with a highly attenuated, Select Agent-excludedpurMdeletion mutant ofB. pseudomallei(strain Bp82) and then subjected to intranasal challenge with virulentB. pseudomalleistrain 1026b. Immunization with Bp82 generated significant protection from challenge withB. pseudomallei, and protection was associated with a significant reduction in bacterial burden in lungs, liver, and spleen of immunized mice. Humoral immunity was critically important for vaccine-induced protection, as mice lacking B cells were not protected by immunization and serum from Bp82-vaccinated mice could transfer partial protection to nonvaccinated animals. In contrast, vaccine-induced protective immunity was found to be independent of both CD4 and CD8 T cells. Tracking studies demonstrated uptake of the Bp82 vaccine strain predominately by neutrophils in vaccine-draining lymph nodes and by smaller numbers of dendritic cells (DC) and monocytes. We concluded that protection following cutaneous immunization with a live attenuatedBurkholderiavaccine strain was dependent primarily on generation of effective humoral immune responses.

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32

Tomic, Adriana, Andrew J. Pollard y Mark M. Davis. "Systems Immunology: Revealing Influenza Immunological Imprint". Viruses 13, n.º 5 (20 de mayo de 2021): 948. http://dx.doi.org/10.3390/v13050948.

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Understanding protective influenza immunity and identifying immune correlates of protection poses a major challenge and requires an appreciation of the immune system in all of its complexity. While adaptive immune responses such as neutralizing antibodies and influenza-specific T lymphocytes are contributing to the control of influenza virus, key factors of long-term protection are not well defined. Using systems immunology, an approach that combines experimental and computational methods, we can capture the systems-level state of protective immunity and reveal the essential pathways that are involved. New approaches and technological developments in systems immunology offer an opportunity to examine roles and interrelationships of clinical, biological, and genetic factors in the control of influenza infection and have the potential to lead to novel discoveries about influenza immunity that are essential for the development of more effective vaccines to prevent future pandemics. Here, we review recent developments in systems immunology that help to reveal key factors mediating protective immunity.

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33

Seo, Sang Heui, Malik Peiris y Robert G. Webster. "Protective Cross-Reactive Cellular Immunity to Lethal A/Goose/Guangdong/1/96-Like H5N1 Influenza Virus Is Correlated with the Proportion of Pulmonary CD8+ T Cells Expressing Gamma Interferon". Journal of Virology 76, n.º 10 (15 de mayo de 2002): 4886–90. http://dx.doi.org/10.1128/jvi.76.10.4886-4890.2002.

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ABSTRACT A/Goose/Guangdong/1/96-like H5N1 influenza viruses now circulating in southeastern China differ genetically from the H5N1 viruses transmitted to humans in 1997 but were their precursors. Here we show that the currently circulating H9N2 influenza viruses provide chickens with cross-reactive protective immunity against the currently circulating H5N1 influenza viruses and that this protective immunity is closely related to the percentage of pulmonary CD8+ T cells expressing gamma interferon (IFN-γ). In vivo depletion of T-cell subsets showed that the cross-reactive immunity was mediated by T cells bearing CD8+ and T-cell receptor (TCR) α/β and that the Vβ1 subset of TCR α/β T cells had a dominant role in protective immunity. The protective immunity induced by infection with H9N2 virus declined with time, lasting as long as 100 days after immunization. Shedding of A/Goose/Guangdong/1/96-like H5N1 virus by immunized chickens also increased with the passage of time and thus may play a role in the perpetuation and spread of these highly pathogenic H5N1 influenza viruses. Our findings indicate that pulmonary cellular immunity may be very important in protecting naïve natural hosts against lethal influenza viruses.

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34

Hogarth, Philip J., Mark J. Taylor y Albert E. Bianco. "IL-5-Dependent Immunity to Microfilariae Is Independent of IL-4 in a Mouse Model of Onchocerciasis". Journal of Immunology 160, n.º 11 (1 de junio de 1998): 5436–40. http://dx.doi.org/10.4049/jimmunol.160.11.5436.

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Abstract Th2 lymphocyte responses under the control of IL-4 and IL-5 are frequently associated with protective responses to parasitic helminths. Studies on the role of these cytokines in acquired resistance to parasitic nematodes indicate that, in the case of gastrointestinal nematodes, immunity is mediated by IL-4, while immunity to tissue-dwelling nematodes is dependent on IL-5. Here we investigate the role of IL-5 and eosinophils in protective immunity to Onchocerca microfilariae in IL-4-deficient mice. In the absence of IL-4, and despite the up-regulation of Th1-type responses, immunity remains dependent on IL-5 and eosinophils. Protection was unaffected by the absence of Ab in B cell-deficient mice, confirming that IL-5 is not acting via either B cell differentiation, Ag presentation, or isotype switching mechanisms. These data demonstrate the dissociation of IL-4 and IL-5 in a functional model of protective immunity to a tissue dwelling nematode and cast doubt on the role of IL-4 in the generation of CD4+ T cell-mediated, IL-5-dependent immunity to Onchocerca microfilariae. Importantly, they also segregate T cell-mediated mechanisms of protective immunity from those characterized in ocular pathologic responses in onchocerciasis, which are dependent on IL-4.

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35

Kollmann, Tobias R., Arnaud Marchant y Sing Sing Way. "Vaccination strategies to enhance immunity in neonates". Science 368, n.º 6491 (7 de mayo de 2020): 612–15. http://dx.doi.org/10.1126/science.aaz9447.

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Neonates are particularly susceptible to infection. This vulnerability occurs despite their responsiveness to most vaccines. However, current vaccines do not target the pathogens responsible for most of the severe neonatal infections, and the time it takes to induce protective pathogen-specific immunity after vaccination limits protection in the first days to weeks of life. Alternative strategies include using vaccines to broadly stimulate neonatal immunity in a pathogen-agnostic fashion or vaccinating women during pregnancy to induce protective antibodies that are vertically transferred to offspring within their window of vulnerability. Protection may be further improved by integrating these approaches, namely vaccinating the neonate under the cover of vertically transferred maternal immunity. The rationale for and knowledge gaps related to each of these alternatives are discussed.

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36

Blander, S. J. y M. A. Horwitz. "Vaccination with the major secretory protein of Legionella induces humoral and cell-mediated immune responses and protective immunity across different serogroups of Legionella pneumophila and different species of Legionella." Journal of Immunology 147, n.º 1 (1 de julio de 1991): 285–91. http://dx.doi.org/10.4049/jimmunol.147.1.285.

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Abstract In a previous study, we demonstrated that immunization of guinea pigs with the major secretory protein (MSP) of Legionella pneumophila, serogroup 1 induced humoral and cell-mediated immune responses to MSP and protective immunity against lethal aerosol challenge with this serogroup of L. pneumophila. Although serogroup 1 L. pneumophila cause most cases of Legionnaires' disease, other serogroups of L. pneumophila and species of Legionella cause many cases. In this study, we have examined if immunization with MSP induces humoral and cell-mediated immune responses and protective immunity across different serogroups of L. pneumophila and species of Legionella. By immunoblot analysis, MSP from L. pneumophila serogroup 1 (Lp1 MSP), L. pneumophila serogroup 6 (Lp6 MSP), and Legionella bozemanii (Lb MSP) shared common epitopes recognized by guinea pig anti-Lp1 MSP antiserum. These MSP molecules, however, were not identical as they had different apparent m.w. Immunization of guinea pigs with MSP induced strong cell-mediated immune responses across the different serogroups and species, as indicated by splenic lymphocyte proliferation and cutaneous delayed-type hypersensitivity in response to both homologous and heterologous MSP. Immunization with MSP induced strong protective immunity across two serogroups of L. pneumophila; overall, 9 survived aerosol challenge with L. pneumophila serogroup 1 compared to 0 of 12 (0%) sham-immunized control animals (p = 3 x 10(-4), Cochran-Mantel-Haenzel chi 2 statistic for pooled data). Immunization with MSP also induced protective immunity across species of Legionella but protection was species-specific. Whereas immunization with Lb MSP induced protective immunity against L. pneumophila, neither immunization with Lp1 MSP nor immunization with Lb MSP induced protective immunity against L. bozemanii, which produces MSP. Not surprisingly, immunization with MSP did not induce protective immunity against MSP-negative Legionella micdadei. In the case of both L. bozemanii and L. micdadei, immunization with a sublethal dose did confer protective immunity to aerosol challenge indicating that these species do contain immunoprotective components. This study demonstrates that immunization with MSP induces humoral and cell-mediated immune responses across different serogroups of L. pneumophila and species of Legionella, but that the capacity of MSP immunization to induce protective immunity is species-specific. Nevertheless, an MSP vaccine has the potential to induce protective immunity against the great majority of cases of Legionnaires' disease.

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Msema Bwire, George y Kennedy Daniel Mwambete. "Immunological Perspectives of sub-Saharan Populations under Prophylaxis against Malaria". Immunology and Inflammation Diseases Therapy 3, n.º 1 (20 de agosto de 2019): 01–03. http://dx.doi.org/10.31579/2637-8876/013.

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Immunity is the state of protection against infectious disease conferred either through an immune response generated by immunization or previous infection. Generated immune responses may be long lasting even lifelong or gives immediate, but short-lived protection. In malaria-endemic areas, young children and pregnant women are particularly susceptible to malaria, but with exposures protective immunity against malaria develop although sterile immunity is never achieved. Assuring protection to vulnerable populations, prophylaxis against malaria is advocated to pregnancy women and sickle cell disease children. Unfortunately, prophylaxis has been suggested to cause a decrease in exposure that curtails the development of acquired protective immunity, leaving individuals more susceptible to malaria in future. To describe this event, a review on effects of intermittent preventive therapy in pregnant women primigravidae (first pregnancy) in particular and chemoprophylaxis against malaria in sickle cell disease children was conducted.

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Mitsuyama, Masao. "Protective immunity against intracellular Parasitic bacteria." Japanese journal of leprosy 69, n.º 2 (2000): 83–86. http://dx.doi.org/10.5025/hansen.69.83.

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Korb, Vanessa, Anil Chuturgoon y Devapregasan Moodley. "Mycobacterium tuberculosis: Manipulator of Protective Immunity". International Journal of Molecular Sciences 17, n.º 3 (25 de febrero de 2016): 131. http://dx.doi.org/10.3390/ijms17030131.

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40

Gupta, Anurag, Anu Sharma, Lotta von Boehmer, Laura Surace, Alexander Knuth y Maries van den Broek. "Radiotherapy supports protective tumor-specific immunity". OncoImmunology 1, n.º 9 (diciembre de 2012): 1610–11. http://dx.doi.org/10.4161/onci.21478.

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41

Rothman, Alan L. "Dengue: defining protective versus pathologic immunity". Journal of Clinical Investigation 113, n.º 7 (1 de abril de 2004): 946–51. http://dx.doi.org/10.1172/jci21512.

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42

Moss, Bernard. "Smallpox vaccines: targets of protective immunity". Immunological Reviews 239, n.º 1 (28 de diciembre de 2010): 8–26. http://dx.doi.org/10.1111/j.1600-065x.2010.00975.x.

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AKAI, PETER S., SWANGJAI PUNGPAK, VIROJ KITIKOON, DANAI BUNNAG y A. DEAN BEFUS. "Possible protective immunity in human opisthorchiasis". Parasite Immunology 16, n.º 6 (junio de 1994): 279–88. http://dx.doi.org/10.1111/j.1365-3024.1994.tb00350.x.

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44

Chang, Mi Ra, Venkatasubramanian Dharmarajan, Christelle Doebelin, Ruben D. Garcia-Ordonez, Scott J. Novick, Dana S. Kuruvilla, Theodore M. Kamenecka y Patrick R. Griffin. "Synthetic RORγt Agonists Enhance Protective Immunity". ACS Chemical Biology 11, n.º 4 (25 de enero de 2016): 1012–18. http://dx.doi.org/10.1021/acschembio.5b00899.

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45

Holz, Lauren E., Daniel Fernandez-Ruiz y William R. Heath. "Protective immunity to liver-stage malaria". Clinical & Translational Immunology 5, n.º 10 (octubre de 2016): e105. http://dx.doi.org/10.1038/cti.2016.60.

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46

de Souza, J. B. "Protective immunity against malaria after vaccination". Parasite Immunology 36, n.º 3 (18 de febrero de 2014): 131–39. http://dx.doi.org/10.1111/pim.12086.

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47

Lagergård, T. "Haemophilus ducreyi: pathogenesis and protective immunity". Trends in Microbiology 3, n.º 3 (marzo de 1995): 87–92. http://dx.doi.org/10.1016/s0966-842x(00)88888-5.

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Fidel, P. L. y J. D. Sobel. "Protective immunity in experimental Candida vaginitis". Research in Immunology 149, n.º 4-5 (mayo de 1998): 361–73. http://dx.doi.org/10.1016/s0923-2494(98)80760-8.

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49

Eldesoky, Ayman, Youssef Mosaad, Yahia Zakria y Samah Hamdy. "Protective immunity after hepatitis B vaccination". Arab Journal of Gastroenterology 10, n.º 2 (junio de 2009): 68–71. http://dx.doi.org/10.1016/j.ajg.2009.05.002.

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50

Wozniak, Karen L., Sarah Hardison, Michal Olszewski y Floyd L. Wormley. "Induction of Protective Immunity Against Cryptococcosis". Mycopathologia 173, n.º 5-6 (6 de diciembre de 2011): 387–94. http://dx.doi.org/10.1007/s11046-011-9505-8.

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