scholarly journals THE ANALYSIS OF SPECIFIC IMMUNE RESPONSE FOR BORRELIA BURGDORFERI ACCORDING TO IN VIVO ANTIGENS IN REGARD TO SYMPTOMS SUBIECTIVELY PERCEIVED BY FORESTERS

2014 ◽  
Vol 1 ◽  
pp. 32-38
Author(s):  
Małgorzata Tokarska-Rodak ◽  
Maria Kozioł-Montewka ◽  
Dorota Plewik ◽  
Justyna Paszkiewicz ◽  
Adam Szepeluk ◽  
...  
Keyword(s):  
Immune Response ◽  
Borrelia Burgdorferi ◽  
Specific Immune Response

scholarly journals Reduced Immune Response to Borrelia burgdorferi in the Absence of γδ T Cells

2011 ◽  
Vol 79 (10) ◽  
pp. 3940-3946 ◽  
Author(s):  
Cuixia Shi ◽  
Bikash Sahay ◽  
Jennifer Q. Russell ◽  
Karen A. Fortner ◽  
Nicholas Hardin ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Borrelia Burgdorferi ◽  
Adaptive Immune Response ◽  
Γδ T Cells ◽  
Content Type ◽  
Adaptive Immune ◽  
Cytokines And Chemokines

ABSTRACTLittle is known regarding the function of γδ T cells, although they accumulate at sites of inflammation in infections and autoimmune disorders. We previously observed that γδ T cellsin vitroare activated byBorrelia burgdorferiin a TLR2-dependent manner. We now observe that the activated γδ T cells can in turn stimulate dendritic cellsin vitroto produce cytokines and chemokines that are important for the adaptive immune response. This suggested thatin vivoγδ T cells may assist in activating the adaptive immune response. We examined this possibilityin vivoand observed that γδ T cells are activated and expand in number duringBorreliainfection, and this was reduced in the absence of TLR2. Furthermore, in the absence of γδ T cells, there was a significantly blunted response of adaptive immunity, as reflected in reduced expansion of T and B cells and reduced serum levels of anti-Borreliaantibodies, cytokines, and chemokines. This paralleled a greaterBorreliaburden in γδ-deficient mice as well as more cardiac inflammation. These findings are consistent with a model of γδ T cells functioning to promote the adaptive immune response during infection.

Simultaneous in vivo tracking of dendritic cells and priming of an antigen-specific immune response

Biomaterials ◽  
2011 ◽  
Vol 32 (26) ◽  
pp. 6254-6263 ◽  
Author(s):  
Young-Woock Noh ◽  
Yong-Suk Jang ◽  
Kook-Jin Ahn ◽  
Yong Taik Lim ◽  
Bong Hyun Chung
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Specific Immune Response

scholarly journals C-Terminal Invariable Domain of VlsE May Not Serve as Target for Protective Immune Response against Borrelia burgdorferi

2001 ◽  
Vol 69 (3) ◽  
pp. 1337-1343 ◽  
Author(s):  
Fang Ting Liang ◽  
Mary B. Jacobs ◽  
Mario T. Philipp
Keyword(s):  
Immune Response ◽  
Borrelia Burgdorferi ◽  
Antigenic Variation ◽  
Keyhole Limpet Hemocyanin ◽  
Protective Immune Response ◽  
Variable Surface ◽  
Entire Sequence ◽  
Mouse Antibody

ABSTRACT VlsE, the variable surface antigen of the Lyme disease spirochete,Borrelia burgdorferi, contains two invariable domains, at the amino and carboxyl termini, respectively, which collectively account for approximately one-half of the entire molecule's length and remain unchanged during antigenic variation. It is not known if these two invariable domains are exposed at the surface of either the antigen or the spirochete. If they are exposed at the spirochete's surface, they may elicit a protective immune response against B. burgdorferi and serve as vaccine candidates. In this study, a 51-mer synthetic peptide that reproduced the entire sequence of the C-terminal invariable domain of VlsE was conjugated to the carrier keyhole limpet hemocyanin and used to immunize mice. Generated mouse antibody was able to immunoprecipitate native VlsE extracted from cultured B. burgdorferi B31 spirochetes, indicating that the C-terminal invariable domain was exposed at the antigen's surface. However, this domain was inaccessible to antibody binding at the surface of cultured intact spirochetes, as demonstrated by both an immunofluorescence experiment and an in vitro killing assay. Mouse antibody to the C-terminal invariable domain was not able to confer protection against B. burgdorferi infection, indicating that this domain was unlikely exposed at the spirochete's surface in vivo. We concluded that the C-terminal invariable domain was exposed at the antigen's surface but not at the surface of either cultured or in vivo spirochetes and thus cannot elicit protection against B. burgdorferi infection.

scholarly journals Toxoplasma gondii Antigen-Pulsed-Dendritic Cell-Derived Exosomes Induce a Protective Immune Response against T. gondii Infection

2004 ◽  
Vol 72 (7) ◽  
pp. 4127-4137 ◽  
Author(s):  
Fleur Aline ◽  
Daniel Bout ◽  
Sébastian Amigorena ◽  
Philippe Roingeard ◽  
Isabelle Dimier-Poisson
Keyword(s):  
Immune Response ◽  
Toxoplasma Gondii ◽  
Ex Vivo ◽  
Specific Immune Response ◽  
Histocompatibility Complex ◽  
Pulsed Dc ◽  
Life Threatening ◽  
Protection Against Infection ◽  
Antigen Presenting

ABSTRACT It was previously demonstrated that immunizing mice with spleen dendritic cells (DCs) that had been pulsed ex vivo with Toxoplasma gondii antigens triggers a systemic Th1-biased specific immune response and induces protection against infection. T. gondii can cause severe sequelae in the fetuses of mothers who acquire the infection during pregnancy, as well as life-threatening neuropathy in immunocompromised patients, in particular those with AIDS. Here, we investigate the efficacy of a novel cell-free vaccine composed of DC exosomes, which are secreted antigen-presenting vesicles that express functional major histocompatibility complex class I and II and T-cell-costimulatory molecules. They have already been shown to induce potent antitumor immune responses. We investigated the potential of DC2.4 cell line-derived exosomes to induce protective immunity against toxoplasmosis. Our data show that most adoptively transferred T. gondii-pulsed DC-derived exosomes were transferred to the spleen, elicited a strong systemic Th1-modulated Toxoplasma-specific immune response in vivo, and conferred good protection against infection. These findings support the possibility that DC-derived exosomes can be used for T. gondii immunoprophylaxis and for immunoprophylaxis against many other pathogens.

scholarly journals The Failure of Immune Response Evasion by Linear Plasmid 28-1-Deficient Borrelia burgdorferi Is Attributable to Persistent Expression of an Outer Surface Protein

2008 ◽  
Vol 76 (9) ◽  
pp. 3984-3991 ◽  
Author(s):  
Monica E. Embers ◽  
Xavier Alvarez ◽  
Tara Ooms ◽  
Mario T. Philipp
Keyword(s):  
Immune Response ◽  
Borrelia Burgdorferi ◽  
Outer Surface ◽  
Time Course ◽  
Surface Protein ◽  
Etiologic Agent ◽  
Linear Plasmid ◽  
Mammalian Host ◽  
Outer Surface Protein

ABSTRACT Infectivity and persistence by Borrelia burgdorferi, the etiologic agent of Lyme disease, rely stringently on regulatory events. Among these is the downregulation of lipoprotein antigen expression, exemplified by outer surface protein C (OspC), at the advent of specific immunity in the mammalian host. B. burgdorferi spirochetes that lack the linear plasmid 28-1 (lp28-1) succumb to the host's immune response. We thus explored the notion that these two phenomena were related—that lp28-1− organisms fail to downregulate ospC and thus are cleared following the appearance of anti-OspC antibody in the murine host. The lp-28-1− isolate and a wild-type (wt) isolate bearing the complete set of plasmids were grown in dialysis membrane chambers that were implanted into rat peritoneal cavities. Analysis of mRNA and protein from these cultures showed that OspC expression levels by lp28-1− organisms are abnormally high in vivo. A time course analysis of ospC expression in tissues following infection indicates also that temporal diminution of the dominant antigen OspC is impaired in lp28-1− spirochetes. Finally, passive transfer of monoclonal OspC-specific antibody into SCID mice 8 days postinfection cleared lp28-1− spirochetes, yet the wt organisms persisted in a majority of animals. These findings indicate that incomplete repression of OspC by lp28-1− organisms renders them susceptible to immune-mediated clearance. The lp28-1 plasmid must harbor one or more genes involved in OspC downregulation.

Cyclophosphamide enhances the release of tumor exosomes that elicit a specific immune response in vivo in a murine T-cell lymphoma

Vaccine ◽  
2019 ◽  
Vol 37 (12) ◽  
pp. 1565-1576 ◽  
Author(s):  
Federico Cocozza ◽  
Florencia Menay ◽  
Rodrigo Tsacalian ◽  
Analía Elisei ◽  
Pura Sampedro ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cell ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Specific Immune Response ◽  
Tumor Exosomes
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