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Analysis of T‐cell hybridomas with an unusual MHC class II‐dependent ligand specificity
Author(s) -
MENDIRATTA S. K.,
SINGH N.,
BAL V.,
Rath S.
Publication year - 1996
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1996.d01-739.x
Subject(s) - ligand (biochemistry) , mhc class ii , major histocompatibility complex , biology , class (philosophy) , mhc class i , microbiology and biotechnology , b cell , chemistry , genetics , immune system , antibody , receptor , computer science , artificial intelligence
We have characterized two unusual T‐cell hybridomas, 1E3 and 3B8, from H‐2 k mice immunized with I‐A b ‐transfected L cells (H‐2 k ), that are stimulated by L cells transfected with I‐A b , I‐A k or I‐E b , but not by non‐transfected L cells. These hybridomas could not be stimulated by spleen cells from H‐2 i3 , H‐2 k , H‐2 b or H‐2 d mice. Monoclonal anti‐I‐A antibodies did not block their responses, suggesting that mouse major histocompatibility complex (MHC) class II molecules may be peptide donors rather than restriction elements for them. The stimulation of these hybridomas by fibroblast targets was not blocked by an anti‐H‐2k k ,D k ‐specific monoclonal antibody. Lipopolysaccharide (LPS)‐activated splenic and peritoneal exudate cells from H‐2 k , H‐2 d , H‐2 i3 , H‐2 b as well as β 2 ‐microglobulin‐deficient, TAP‐1‐deficient and I‐Aα‐deficient H‐2 b mice stimulated these hybridomas. LPS could also activate a macrophage cell line, but not a B‐cell line, to become stimulatory for 1E3. A rat antiserum against untransfected L cells specifically and significantly blocked the response of 1E3. Thus, 1E3 may recognize a conserved murine MHC class II peptide loaded in a TAP‐1‐independent fashion on a non‐classical, monomorphic, β 2 ‐microglobulin‐independent restriction element.