scholarly journals S-Layer From Lactobacillus brevis Modulates Antigen-Presenting Cell Functions via the Mincle-Syk-Card9 Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Mariano Prado Acosta ◽  
Guillaume Goyette-Desjardins ◽  
Jörg Scheffel ◽  
Anne Dudeck ◽  
Jürgen Ruland ◽  
...  
Keyword(s):  
T Cell ◽  
Inflammatory Cytokines ◽  
Lactobacillus Brevis ◽  
Antigen Presenting Cell ◽  
Lectin Receptors ◽  
Gm Csf ◽  
Cell Functions ◽  
Key Factor ◽  
Anti Inflammatory ◽  
Antigen Presenting

C-type lectin receptors (CLRs) are pattern recognition receptors that are crucial in the innate immune response. The gastrointestinal tract contributes significantly to the maintenance of immune homeostasis; it is the shelter for billions of microorganisms including many genera of Lactobacillus sp. Previously, it was shown that host-CLR interactions with gut microbiota play a crucial role in this context. The Macrophage-inducible C-type lectin (Mincle) is a Syk-coupled CLR that contributes to sensing of mucosa-associated commensals. In this study, we identified Mincle as a receptor for the Surface (S)-layer of the probiotic bacteria Lactobacillus brevis modulating GM-CSF bone marrow-derived cells (BMDCs) functions. We found that the S-layer/Mincle interaction led to a balanced cytokine response in BMDCs by triggering the release of both pro- and anti-inflammatory cytokines. In contrast, BMDCs derived from Mincle−/−, CARD9−/− or conditional Syk−/− mice failed to maintain this balance, thus leading to an increased production of the pro-inflammatory cytokines TNF and IL-6, whereas the levels of the anti-inflammatory cytokines IL-10 and TGF-β were markedly decreased. Importantly, this was accompanied by an altered CD4+ T cell priming capacity of Mincle−/− BMDCs resulting in an increased CD4+ T cell IFN-γ production upon stimulation with L. brevis S-layer. Our results contribute to the understanding of how commensal bacteria regulate antigen-presenting cell (APC) functions and highlight the importance of the Mincle/Syk/Card9 axis in APCs as a key factor in host-microbiota interactions.

scholarly journals Differential Impact of PD-1 and/or Interleukin-10 Blockade on HIV-1-Specific CD4 T Cell and Antigen-Presenting Cell Functions

2013 ◽  
Vol 88 (5) ◽  
pp. 2508-2518 ◽  
Author(s):  
F. Porichis ◽  
M. G. Hart ◽  
J. Zupkosky ◽  
L. Barblu ◽  
D. S. Kwon ◽  
...  
Keyword(s):  
T Cell ◽  
Interleukin 10 ◽  
Cd4 T Cell ◽  
Differential Impact ◽  
Antigen Presenting Cell ◽  
Cell Functions ◽  
Antigen Presenting ◽  
Hiv 1

Downregulation of Antigen-Presenting Cell Functions After Administration of Mitogenic Anti-CD3 Monoclonal Antibodies in Mice

Blood ◽  
1999 ◽  
Vol 94 (12) ◽  
pp. 4347-4357 ◽  
Author(s):  
Eric Muraille ◽  
Fabienne Andris ◽  
Bernard Pajak ◽  
K. Martin Wissing ◽  
Thibaut De Smedt ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
T Cell Activation ◽  
Immunosuppressive Agents ◽  
Interleukin 12 ◽  
Spleen Cells ◽  
Antigen Presenting Cell ◽  
Cell Functions ◽  
Antigen Presenting

Abstract Antibodies against CD3ɛ are widely used as immunosuppressive agents. Although it is generally assumed that these reagents exert their immunomodulatory properties by inducing T-cell deletion and/or inactivation, their precise mechanism of action remains to be elucidated. Using a murine model, we demonstrate in this report that administration of anti-CD3ɛ antibodies causes the migration and maturation of dendritic cells (DC) in vivo, as determined by immunohistochemical analysis. This maturation/migration process was followed by selective loss of splenic DC, which resulted in a selective inhibition of antigen-presenting cell (APC) functions in vitro. Spleen cells from anti-CD3ɛ–treated animals were unable to productively stimulate naive alloreactive T cells and Th1-like clones in response to antigen, while retaining the ability to present antigen to a T-cell hybridoma and Th2 clones. Anti-CD3ɛ treatment was found to induce a selective deficiency in the ability of spleen cells to produce bioactive interleukin-12 in response to CD40 stimulation. APC dysfunction was not observed when nonmitogenic forms of anti-CD3ɛ antibodies were used, suggesting that splenic DC loss was a consequence of in vivo T-cell activation. Nonmitogenic anti-CD3ɛ monoclonal antibodies were found to be less immunosuppressive in vivo, raising the possibility that APC dysfunction contributes to anti-CD3ɛ–induced immunomodulation. Collectively, these data suggest a novel mechanism by which mitogenic anti-CD3ɛ antibodies downregulate immune responses.

CD48 Controls T-Cell and Antigen-Presenting Cell Functions in Experimental Colitis

2006 ◽  
Vol 130 (2) ◽  
pp. 424-434 ◽  
Author(s):  
Ana C. Abadía–Molina ◽  
Honbing Ji ◽  
William A. Faubion ◽  
Aimée Julien ◽  
Yvette Latchman ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Colitis ◽  
Antigen Presenting Cell ◽  
Cell Functions ◽  
Antigen Presenting

scholarly journals Anti-Inflammatory Cytokines Directly Inhibit Innate but Not Adaptive CD8+ T Cell Functions

2014 ◽  
Vol 88 (13) ◽  
pp. 7474-7484 ◽  
Author(s):  
B. E. Freeman ◽  
C. Meyer ◽  
M. K. Slifka
Keyword(s):  
T Cell ◽  
Inflammatory Cytokines ◽  
Cd8 T Cell ◽  
Cell Functions ◽  
Anti Inflammatory

Downregulation of Antigen-Presenting Cell Functions After Administration of Mitogenic Anti-CD3 Monoclonal Antibodies in Mice

Blood ◽  
1999 ◽  
Vol 94 (12) ◽  
pp. 4347-4357
Author(s):  
Eric Muraille ◽  
Fabienne Andris ◽  
Bernard Pajak ◽  
K. Martin Wissing ◽  
Thibaut De Smedt ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
T Cell Activation ◽  
Immunosuppressive Agents ◽  
Interleukin 12 ◽  
Spleen Cells ◽  
Antigen Presenting Cell ◽  
Cell Functions ◽  
Antigen Presenting

Antibodies against CD3ɛ are widely used as immunosuppressive agents. Although it is generally assumed that these reagents exert their immunomodulatory properties by inducing T-cell deletion and/or inactivation, their precise mechanism of action remains to be elucidated. Using a murine model, we demonstrate in this report that administration of anti-CD3ɛ antibodies causes the migration and maturation of dendritic cells (DC) in vivo, as determined by immunohistochemical analysis. This maturation/migration process was followed by selective loss of splenic DC, which resulted in a selective inhibition of antigen-presenting cell (APC) functions in vitro. Spleen cells from anti-CD3ɛ–treated animals were unable to productively stimulate naive alloreactive T cells and Th1-like clones in response to antigen, while retaining the ability to present antigen to a T-cell hybridoma and Th2 clones. Anti-CD3ɛ treatment was found to induce a selective deficiency in the ability of spleen cells to produce bioactive interleukin-12 in response to CD40 stimulation. APC dysfunction was not observed when nonmitogenic forms of anti-CD3ɛ antibodies were used, suggesting that splenic DC loss was a consequence of in vivo T-cell activation. Nonmitogenic anti-CD3ɛ monoclonal antibodies were found to be less immunosuppressive in vivo, raising the possibility that APC dysfunction contributes to anti-CD3ɛ–induced immunomodulation. Collectively, these data suggest a novel mechanism by which mitogenic anti-CD3ɛ antibodies downregulate immune responses.

Analysis of Neonatal T Cell and Antigen Presenting Cell Functions

1997 ◽  
Vol 57 (2) ◽  
pp. 69-79 ◽  
Author(s):  
Harsha N Trivedi ◽  
Kent T HayGlass ◽  
Venugopal Gangur ◽  
James G Allardice ◽  
Joanne E Embree ◽  
...  
Keyword(s):  
T Cell ◽  
Antigen Presenting Cell ◽  
Cell Functions ◽  
Antigen Presenting
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