Interleukin 17-producing T helper cells and interleukin 17 orchestrate autoreactive germinal center development in autoimmune BXD2 mice

Interleukin-17 (IL-17), a cytokine associated with inflammation and autoimmunity, may promote autoimmune disease through another mechanism than its proinflammatory effects. Autoimmune BXD2 mice have a stronger expression of IL-17 and spontaneously develop germinal centers (GCs) before an increase in production of pathogenic autoantibodies occurs.

Blocking IL-17 signalling cleaves the CD4+ T-cell and B-cell interactions that are necessary for the formation of GCs. Mice lacking the IL-17 receptor show reduced GC B-cell development and humoral responses.

When IL-17 is produced increased expression of the genes Rgs13 and Rgs16 may be observed. The genes encode for regulators of G-protein signalling. The result is suppression of the B-cell chemotactic response to the chemokine CXCL12. Apparently, IL-17 drives autoimmune responses by promoting the formation of spontaneous GCs.

Related antibodies on antibodies-online.com:

Interleukin-17 (IL-17)

CD4+ T-cells

B-cells

IL-17-Receptors:
IL-17-Receptor B
IL-17-Receptor B/E
IL-17-Receptor D

G-Proteine

CXCL11

CXCL14

Antibodies for the research area chemokines: »Show antibodies

Antibodies for the research area cytokines: »Show antibodies

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