Premium
Spontaneous Proliferation of HTLV‐II‐Infected Peripheral Blood Lymphocytes: HLA‐DR‐Driven, IL‐2‐Dependent Response
Author(s) -
Lal Renu B.,
Hjelle Brian,
Rudolph Donna L.
Publication year - 1992
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1992.tb02088.x
Subject(s) - peripheral blood mononuclear cell , interleukin 2 , immunology , mixed lymphocyte reaction , biology , population , antibody , t lymphocyte , microbiology and biotechnology , antigen , virology , t cell , immune system , in vitro , medicine , biochemistry , environmental health
Peripheral blood lymphocytes obtained from HTLV‐II‐infected persons ( n = 13) and cultured in the absence of exogenous stimulator demonstrated augmented spontaneous proliferation (17,672 ± 5,498 cpm) when compared with cells from healthy donors (1,921 ± 1,306 cpm). Removal of non‐T population did not abrogate the proliferative response of patients' PBMC, suggesting that the proliferation is not related to the autologous mixed lymphocyte reaction. Addition of recombinant interleukin‐2 (rIL‐2; 0.1 U/ml) to spontaneously proliferating cultures from HTLV‐II‐infected persons resulted in a 3‐ to 4‐fold increase in proliferation (61,985 ± 16,003); in contrast, PBMC from controls demonstrated 38‐ to 42‐fold increase in their proliferative capacity in response to rIL‐2 (77,256 ± 13,044). Antibodies to both IL‐2 receptor and HLA‐DR were able to inhibit the spontaneous proliferation of PBMC from HTLV‐II‐infected persons in a dose‐dependent manner. Furthermore, addition of cyclosporin A, which preferentially blocks accumulation of IL‐2 mRNA, also inhibited spontaneous proliferation in a dose‐dependent manner. These observations suggest that the spontaneous proliferation of HTLV‐II‐infected PBMC is at least in part an HLA‐DR‐driven, IL‐2‐dependent event, which is not analogous to the AMLR.