As a note, why couldn’t a finite effector T cell lifespan coupled with the decreasing abundance of the Eliminon itself during an effective ridding response control the magnitude of the effector response? When the Eliminon has been eliminated, T cells specific to that Eliminon no longer become activated and the response winds down. Why is this theoretically check details inadequate requiring one to invoke Treg? 3. While there are descriptions of regulatory T cell populations that mediate some of their suppressive effects through

the secretion of soluble mediators such as IL-10, particularly in the gut, the ‘general description filling the literature’ is not, in fact, that FoxP3+ Treg primarily work nonspecifically through these soluble mediators but rather that they interact with and modulate the function of APC in an antigen- and contact-dependent manner. Using intravital two-photon microscopy, it has been shown that in vivo in lymph nodes, Treg specific for DC-presented antigen readily formed stable interactions with the DCs and were able to inhibit their formation of stable interactions with CD4+ (Tcon) [8, 9]. FoxP3+ Treg constitutively express the co-inhibitory molecule

CTLA-4, which has recently been shown to have the ability to ‘strip’ molecules of CD80 and CD86 off of the cell surface of DCs by a process of trans-endocytosis [10]. Importantly, CTLA-4 is required for FoxP3+ Treg suppressive ability [11, 12] and mice selectively lacking CTLA-4 expression in the FoxP3+ lineage develop severe autoimmune disease [13]. Given that the bulk of in selleck products vivo evidence suggests that the primary means of suppression by FoxP3+Treg is by interfering with Teff cell activation at the immune synapse, I wonder why we couldn’t just treat Treg as another ‘class’, albeit a regulatory one that turns off the response/prevents it? The same mechanisms proposed to maintain coherence Etofibrate and independence of immune responses, despite a single APC-presenting peptides derived

from multiple ‘Eliminons’ requiring discrete effector classes to properly ‘rid’ could also be applied to explain how, simultaneously on the same APC, a regulatory response to a single ‘non-Eliminon’ and an effector response to an Eliminon could remain discrete. “
“IL-15 is an essential survival factor for CD8αα+ intestinal intraepithelial lymphocytes (iIELs) in vitro and in vivo. However, the IL-15-induced survival signals in primary CD8αα+ iIELs remains elusive. Although Bcl-2 level in CD8αα+ iIELs positively correlates with IL-15Rα expression in the intestinal epithelial cells, overexpression of Bcl-2 only moderately restores CD8αα+ γδ iIELs in Il15−/− mice. Here, we found that IL-15 promptly activated a Jak3-Jak1-PI3K-Akt pathway that led to the upregulation of Bcl-2 and Mcl-1.