Everything about Superantigens: Supersignalers? - Science

The biological strength of the SAg (its capability to stimulate) is figured out by its affinity for the TCR. Droops with the greatest affinity for the TCR elicit the greatest reaction. SPMEZ-2 is the most potent SAg found to date. T-cell signaling [modify] The SAg cross-links the MHC and the TCR inducing a signaling path that results in the proliferation of the cell and production of cytokines.

Low levels of Zap-70 have actually been discovered in T-cells triggered by SAgs, suggesting that the normal signaling path of T-cell activation suffers. It is hypothesized that Fyn instead of Lck is activated by a tyrosine kinase, leading to the adaptive induction of anergy. Both the protein kinase C pathway and the protein tyrosine kinase pathways are activated, leading to upregulating production of proinflammatory cytokines.

Direct results [edit] Droop stimulation of antigen presenting cells and T-cells elicits a response that is mainly inflammatory, focused on the action of Th1 T-helper cells. home phototherapy for psoriasis of the significant products are IL-1, IL-2, IL-6, TNF-, gamma interferon (IFN-), macrophage inflammatory protein 1 (MIP-1), MIP-1, and monocyte chemoattractant protein 1 (MCP-1).

Removal or anergy of activated T-cells follows infection. This arises from production of IL-4 and IL-10 from extended direct exposure to the contaminant. The IL-4 and IL-10 downregulate production of IFN-gamma, MHC Class II, and costimulatory molecules on the surface area of APCs. These effects produce memory cells that are unresponsive to antigen stimulation.

MHC crosslinking also triggers a signaling path that suppresses hematopoiesis and upregulates Fas-mediated apoptosis. IFN- is another product of extended SAg direct exposure. This cytokine is closely related to induction of autoimmunity, and the autoimmune disease Kawasaki illness is known to be triggered by Droop infection. Droop activation in T-cells leads to production of CD40 ligand which activates isotype switching in B cells to Ig, G and Ig, M and Ig, E.

The toxic results of the microbe and SAg likewise damage tissue and organ systems, a condition understood as harmful shock syndrome. If the initial swelling is endured, the host cells end up being anergic or are erased, resulting in a severely jeopardized immune system. Superantigenicity independent (indirect) effects [edit] Apart from their mitogenic activity, SAgs have the ability to cause signs that are particular of infection.