2004
DOI: 10.4049/jimmunol.173.5.3305
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TGF-β Receptor Signaling Is Critical for Mucosal IgA Responses

Abstract: TGF-β receptor (TβR) signaling is important for systemic IgA production; however, its contribution to IgA secretion at mucosal sites remained uncertain. This important question was addressed using mice lacking the TβR in B cells (TβRII-B). Although reduced, IgA-secreting cells and IgA were still present in the systemic and mucosal compartments. The adaptive immune response was investigated after oral or nasal immunization using adjuvants acting on different molecular targets, namely, the cholera toxin B subuni… Show more

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Cited by 135 publications
(88 citation statements)
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“…However, to generate high affinity antibodies and long-term memory responses, antigen-presenting cells, B cells, and T follicular helper cells must interact in germinal centers (48,49). T-cell help allows not only class-switching to IgA but also the promotion of ASC and MBC formation (50,51 …”
Section: Discussionmentioning
confidence: 99%
“…However, to generate high affinity antibodies and long-term memory responses, antigen-presenting cells, B cells, and T follicular helper cells must interact in germinal centers (48,49). T-cell help allows not only class-switching to IgA but also the promotion of ASC and MBC formation (50,51 …”
Section: Discussionmentioning
confidence: 99%
“…TGFß has been well defined as crucial for IgA CSR (27). Thus, B cells deficient in TGFßRII Ϫ/Ϫ do not make IgA (11,30) and mice deficient in SMAD2 and SMAD3 signaling factors downstream of the TGFß-R also have deficient IgA responses (13,31). Because multiple cell types can produce TGFß, including epithelial cells, dendritic cells, and non-regulatory helper T cells, which are all well represented in the intestine, the cellular source of TGFß that is needed for IgA CSR has been unclear.…”
Section: Discussionmentioning
confidence: 99%
“…Induction of IgA class switching by TGF-b is associated with increased transcription of a-germline transcripts (Lebman et al 1990;Shockett and Stavnezer 1991) because of binding of activated Smads and Runx3 to a tandem-repeat element in the a-germline transcript promoter (Lin and Stavnezer 1992;Shi and Stavnezer 1998;Hanai et al 1999;Pardali et al 2000;Zhang and Derynck 2000;Park et al 2001). Mice with B-cell-specific loss of TGF-b signaling also show dramatic reductions in serum and mucosal IgA levels (Cazac and Roes 2000;Borsutzky et al 2004). Interestingly, whereas Smad3-deficient mice show relatively normal IgA production (Yang et al 1999), Bcell-specific inactivation of Smad2 expression recapitulates the reduction in IgA observed in mice with TbRII-deficient B cells.…”
Section: Activation and Differentiationmentioning
confidence: 99%