IndraLab

"Rorγt -deficient mice have impaired intestinal SLO development resulting in the absence of mesenteric lymph nodes and Peyer’s and colonic patches, but also have defective cryptopatches and isolated lymphoid follicles. xref , xref While these lymphoid structures are critical to mount appropriate immune responses, LTi-deficient mice are still able to preserve their barrier integrity and to maintain intestinal homeostasis, as TLS development occurs in the colon of Rorγt -deficient mice during inflammation and seems to be dependent on the gut microbiota. xref Similarly, inducible bronchus-associated lymphoid tissue (iBALT) develops in lungs after LPS exposure or influenza-infection in mice lacking SLO. xref , xref In influenza-infectedLta −/- mice, local CXCL13 and CCL21 expression colocalizes with the B cell-rich zone and PNAd-expressing HEVs, respectively, in iBALT. xref Similarly,Rorc −/ − andId2 −/- mice exposed to LPS and infected with influenza also form iBALT. xref Together, these results demonstrate that local inflammation is a principal trigger of TLS formation, and similar mechanisms are likely to occur in tumors. xref These vascular structures together with local chemotactic factors allow the recruitment and accumulation of B and T cells sustaining the initial formation and the assembly of the nascent TLS. xref , xref Overall, while a parallel between SLO and TLS formation occurs, additional molecular and cellular events principally dependent on sustained local inflammation trigger TLS neogenesis."

"In mice that are deficient in G protein ai2 subunit, PPs regress and colitis is observed, emphasizing the importance of G proteins in the formation and retention of SLO and TLS ( xref )."

"While bearing a similar histological structure to SLO, the signals that regulate TLS and SLO formation can diverge, and a series of pro-inflammatory cytokines has been ascribed as responsible for TLS formation at different anatomical sites."

"CXCL13, also known as BLC, is critical for the formation of SLO and TLS."

"While bearing a similar histological structure to SLO, the signals that regulate TLS and SLO formation can diverge and a series of pro-inflammatory cytokines have been ascribed as responsible for TLS formation at different anatomical sites."