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MALT1 Protease Regulates T-Cell Immunity via the mTOR Pathway in Oral Lichen Planus.
- Source :
-
Inflammation . Jun2024, Vol. 47 Issue 3, p939-957. 19p. - Publication Year :
- 2024
-
Abstract
- Oral lichen planus (OLP) is a T cell–mediated immune mucosal disease of unknown pathogenesis. Whether mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), an intracellular signaling protein, is involved in the T-cell immune dysfunction of OLP remains elusive. MALT1 expression in local and peripheral T cells of OLP and controls was analyzed using immunohistochemistry, multiplex immunohistochemistry, and flow cytometry. The expression of MALT1 in activated Jurkat T cells incubated with either OLP plasma or interleukin (IL)-7/IL-15 was determined by flow cytometry. The effects of MALT1 and mechanistic target of rapamycin (mTOR) on T-cell immunity were investigated through western blot, CCK8 assay, and flow cytometry. The expression of MALT1 protein was elevated in local OLP T cells and mucosal-associated invariant T (MAIT) cells, while reduced in peripheral OLP T cells, MAIT cells, and follicular helper-like MAIT (MAITfh) cells. Stimulation with OLP plasma and IL-7/ IL-15 had no effect on MALT1 expression in activated Jurkat T cells. MALT1 protease-specific inhibitor (MI-2) induced mTOR phosphorylation, increased B-cell lymphoma 10 (BCL10) expression, inhibited T-cell proliferation, and promoted T-cell apoptosis. The combination of MI-2 and rapamycin increased MALT1 expression, further suppressed T-cell proliferation, and facilitated T-cell apoptosis. MALT1 expression is aberrant in both local lesions and peripheral blood of OLP. Inhibition of the mTOR pathway further enhances the suppression of T-cell proliferation and the promotion of apoptosis induced by the MALT1 inhibitor MI-2. [ABSTRACT FROM AUTHOR]
- Subjects :
- *ORAL lichen planus
*MUCOSA-associated lymphoid tissue lymphoma
*T cells
Subjects
Details
- Language :
- English
- ISSN :
- 03603997
- Volume :
- 47
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Inflammation
- Publication Type :
- Academic Journal
- Accession number :
- 177624709
- Full Text :
- https://doi.org/10.1007/s10753-023-01952-w