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Identification of HLA class II antigens as the targets of effector clones which may cause transfusion‐associated graft‐versus‐host disease
Author(s) -
Nishimura M.,
Uchida S.,
Mitsunaga S.,
Yahagi Y.,
Nakajima K.,
Tadokoro K.,
Juji T.
Publication year - 1997
Publication title -
transfusion medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.471
H-Index - 59
eISSN - 1365-3148
pISSN - 0958-7578
DOI - 10.1046/j.1365-3148.1997.d01-9.x
Subject(s) - ctl* , clone (java method) , antigen , immunology , cytotoxic t cell , human leukocyte antigen , monoclonal antibody , biology , effector , cytotoxicity , antibody , virology , genetics , gene , in vitro , cd8
We established T cell clones, which were considered to be the possible cause of transfusion‐associated graft‐versus‐host disease (TA‐GVHD), from the peripheral blood lymphocytes (PBLs) of two patients. In both cases, several CD4 + cytotoxic T‐cell (CTL) clones were established. In case I, the target antigen of the established CD4 + clones was a DRB1*0403‐related antigen serologically typed as HLA DR4, which was one of the patient HLA antigens. In case II, the target of four out of five established CD4 + CTL was a DRB1*1302‐related antigen. One CD4 + CTL clone showed cytotoxicity against cells carrying A*2402, B*4403, Cw*1403 and DPB1*0401. A monoclonal antibody (mAb) blocking study showed only anti‐DP mAb inhibited the cytotoxicity of this clone. Thus, it might be considered that this clone recognizes HLA‐DP with its binding peptides derived from either A*2402, B*4403, Cw*1403 or DRB1*1302. Our findings indicate that CD4 + CTLs may play important roles in the aetiology of TA‐GVHD and that the antigens of patients recognized by donor‐derived effector cells may not always recognize a single HLA antigen.