Hypersensitivity Reactions in the Small Intestine

Mowat, A M; Borland, Annette; Parrott, Delphine M. V.

doi:10.1097/00007890-198602000-00012

Cited by 28 publications

(2 citation statements)

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“…Previous reports showed that intestinal IELs respond very poorly to T cell stimuli compared with splenic T cells (Mowat et al, 1986(Mowat et al, , 1989Mosley et al, 1991;Barrett et al, 1992;Gramzinski et al, 1993), yet these cells still possess normal cytotoxic responses (Lefran,ois and Gooman, 1989;Viney et al, 1990;Guy-Grand et al, 1991). Our studies could not demonstrate a proliferative response of r mutant IELs; however, the tumor-induced FceRI-y chainbearing T cells, referred to above, maintain their proliferative responses to T cell stimuli and secrete lymphokines, but have blunted TCR/CD3-dependent Ca2' flux response and abrogated cytotoxicity against the tumor (Mizoguchi et al, 1992).…”

Section: Analyses Of T Cell and Nkmentioning

confidence: 99%

Abnormal T cell development in CD3-zeta-/- mutant mice and identification of a novel T cell population in the intestine.

et al. 1993

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The T cell antigen receptor (TCR)‐associated invariable membrane proteins (CD3‐gamma, ‐delta, ‐epsilon and ‐zeta) are critical to the assembly and cell surface expression of the TCR/CD3 complex and to signal transduction upon engagement of TCR with antigen. Disruption of the CD3‐zeta gene by homologous recombination resulted in a structurally abnormal thymus which primarily contained CD4‐ CD8‐ and TCR/CD3very lowCD4+CD8+ cells. Spleen and lymph nodes of CD3‐zeta‐/‐ mutant mice contained a normal number and ratio of CD4+ and CD8+ single positive cells that were TCR/CD3very low. These splenocytes did not respond to antibody cross‐linking or mitogenic triggering. The V beta genes of CD4‐CD8‐ and CD4+CD8+ thymocytes and splenic T cells were productively rearranged. These data demonstrated that (i) in the absence of the CD3‐zeta chain, the CD4‐ CD8‐ thymocytes could differentiate to CD4+CD8+ TCR/CD3very low thymocytes, (ii) that thymic selection might have occurred, (iii) but that the transition to CD4+CD8‐ and CD4‐CD8+ cells took place at a very low rate. Most strikingly, intraepithelial lymphocytes (IELs) isolated from the small intestine or the colon expressed normal levels of TCR/CD3 complexes on their surface which contained Fc epsilon RI gamma homodimers. In contrast to CD3‐zeta containing IELs, these cells failed to proliferate after triggering with antibody cross‐linking or mitogen. In comparison to thymus‐derived peripheral T cells in the spleen and lymph nodes, the preferential expression of normal levels of TCR/CD3 in intestinal IELs suggested they mature via an independent extrathymic pathway.

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Section: Analyses Of T Cell and Nkmentioning

confidence: 99%

Abnormal T cell development in CD3-zeta-/- mutant mice and identification of a novel T cell population in the intestine.

et al. 1993

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“…Although a different susceptibility to tolerance exists by distinct classes of inflammatory responses, Th1-and Th2-dependent cytokine and antibody responses can be tolerized by a number of regimes [126,[129][130][131][132]. Delayed-type hypersensitivity reactions and Th1-dependent inflammation is more easily suppressed by oral antigen than Th2-dependent antibody formation [84,126,[133][134][135][136]]. An exception is the IL-4-dependent IgE response that is highly susceptible to oral tolerance induction [137][138][139].…”

Section: Il-4-and Il-10-producing Cd4+ T Cellsmentioning

confidence: 99%

Oral Tolerance and TGF-β -Producing Cells

Faria¹,

Weiner²

2006

IADT

100

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Multiple mechanisms have been proposed to explain the immune hyporesponsiveness to fed antigens, a phenomenon named oral tolerance. Low doses of orally administered antigen are reported to favor active suppression with the generation of regulatory cells, whereas high doses would favor clonal anergy/deletion. A major conceptual advance in oral tolerance has been the demonstration that TGF-beta plays a central role in oral tolerance as a mediator secreted by Th3 cells. In addition, recent pieces of evidence suggest that TGF-beta may be a primary link between distinct populations of regulatory T cells that are induced by feeding. Conversion of CD4+CD25- into CD4+CD25+ T cells by the expression of FoxP3 involves TGF-beta. A membrane-bound form of TGF-beta (containing latency-associated peptide - LAP) has also been described and LAP+ CD4+ T cells mediate suppression in the gut by a TGF-beta-dependent mechanism. Most of these regulatory T cells are anergic cells indicating that anergy may be also related to Treg induction. Moreover, deletional events taking place in the gut mucosa induce TGF-beta production by either macrophages that phagocyte apoptotic cells or by the dying T cells. Thus, it appears that TGF-beta-producing cells are not only crucial for oral tolerance, but they may be master regulators of most of the mechanisms triggered by antigen feeding.

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The Role of Antigen Processing and Suppressor T Cells in Immune Responses to Dietary Proteins in Mice

Mowat

Lamont

Ströbel³

et al. 1987

Recent Advances in Mucosal Immunology

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Hypersensitivity Reactions in the Small Intestine

Cited by 28 publications

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Abnormal T cell development in CD3-zeta-/- mutant mice and identification of a novel T cell population in the intestine.

Abnormal T cell development in CD3-zeta-/- mutant mice and identification of a novel T cell population in the intestine.

Oral Tolerance and TGF-β -Producing Cells

The Role of Antigen Processing and Suppressor T Cells in Immune Responses to Dietary Proteins in Mice

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Hypersensitivity Reactions in the Small Intestine

Cited by 28 publications

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Abnormal T cell development in CD3-zeta-/- mutant mice and identification of a novel T cell population in the intestine.

Abnormal T cell development in CD3-zeta-/- mutant mice and identification of a novel T cell population in the intestine.

Oral Tolerance and TGF-&#946; -Producing Cells

The Role of Antigen Processing and Suppressor T Cells in Immune Responses to Dietary Proteins in Mice

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Oral Tolerance and TGF-β -Producing Cells