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Inhibitory Effects of Anti‐HLA‐A, B, C Heavy Chain and Anti‐β 2 Microglobulin Monoclonal Antibodies on Alloantigen and Microbial Antigen‐Induced Immune Responses in Vitro
Author(s) -
SPAGNOLI G. C.,
AUSIELLO C. M.,
CASSONE A.,
CASCIANI C. U.,
BELLONE G.,
MALAVASI F.
Publication year - 1987
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1987.tb01081.x
Subject(s) - antigen , monoclonal antibody , immune system , epitope , cytotoxic t cell , biology , human leukocyte antigen , immunology , major histocompatibility complex , antibody , lymphocyte , t lymphocyte , microbiology and biotechnology , in vitro , chemistry , biochemistry
The role of HLA class I subunits in class Il‐restricted immune responses was investigated by means of a panel of monoclonal antibodies (MoAb) recognizing HLA‐A,B,C heavy chain and different β 2 mitroglobulin (β 2 m) epitopes. MoAb against either class I subunit strongly inhibited mixed lymphocyte cultures, generation of cytotoxic T lymphocyte cultures, generation of cytotoxic T lymphoytes or natural killer‐like activity, and lymphoproliferation in response lo soluble or particulate microbial antigens derived from Candida alhicans . In general. anti‐β 2 m MoAb were more efficient inhibitors than anti‐HLA‐A, B, C heavy chain MoAb. The inhibitory effects were specific, in that the parental myeloma ascitic fluid or a low‐affinity MoAb against β 2 m, or MoAh directed against non‐HLA surface structures did not affect any of the immune responses studied. The MoAb‐induced inhibition could not be attributed to nonspecific toxic effects, since PHA‐induced blastogenesis and lL‐2‐dependent proliferation of mixed lymphocyte culture (MLC) blasts were not inhibited. Furthermore, exogenous IL‐2 did not reverse the block of MLC and microbial antigen‐induced proliferative responses by MoAb. Taken together, these data suggest an involvement ol both subunits of class I antigens in class II‐resiticted inmiune reponses.