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Tumor-infiltrating mucosal-associated invariant T (MAIT) cells retain expression of cytotoxic effector molecules.

Artikel i vetenskaplig tidskrift
Författare Patrik Sundström
Louis Szeponik
Filip Ahlmanner
Malin Sundquist
Justin S B Wong
Elinor Bexe-Lindskog
Bengt I. Gustafsson
Marianne Quiding-Järbrink
Publicerad i Oncotarget
Volym 10
Nummer/häfte 29
Sidor 2810-2823
ISSN 1949-2553
Publiceringsår 2019
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för kirurgi
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 2810-2823
Språk en
Länkar dx.doi.org/10.18632/oncotarget.2686...
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämneskategorier Immunologi inom det medicinska området

Sammanfattning

Mucosal-associated invariant T (MAIT) cells all express a semi-invariable T cell receptor recognizing microbial metabolites presented on the MHC class I-like molecule MR1. Upon activation, they rapidly secrete cytokines and increase their cytotoxic potential. We showed recently that MAIT cells with Th1 phenotype accumulate in human colon adenocarcinomas. Here, we investigated the cytotoxic potential of tumor-infiltrating MAIT cells in colon adenocarcinomas, and to what extent it may be affected by the tumor microenvironment. Activation of MAIT cells from tumors induced increased Granzyme B, and to a lesser extent, perforin expression. Degranulation was assessed by surface expression of CD107a, and was also seen in response to cognate antigen recognition. The cytotoxic potential of tumor-associated MAIT cells was very similar to that of MAIT cells from unaffected colon. MAIT cells were also identified by immunofluorescence in direct contact with tumor cells in sections from colon cancer specimens. To summarize, tumor-associated MAIT cells from colon tumors have strong cytotoxic potential and are not compromised in this regard compared to MAIT cells from the unaffected colon. We conclude that MAIT cells may contribute significantly to the protective immune response to tumors, both by secretion of Th1-associated cytokines and by direct killing of tumor cells.

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