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Antigen‐Specific Proliferative Response of Peritoneal Exudate Lymphocytes Primed with Antigen and Bacterial Lipopolysaccharide: The Roles of Ia + Accessory Cells and IL‐2
Author(s) -
Nitta Toshimasa,
Imai Hiroaki,
Ogasawara Yuko,
Hirayama Nobukuni,
Nakano Masayasu
Publication year - 1993
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.1348-0421.1993.tb01729.x
Subject(s) - antigen , lipopolysaccharide , biology , microbiology and biotechnology , population , t lymphocyte , cytotoxic t cell , antigen presenting cell , cd40 , t cell , immunology , in vitro , immune system , medicine , biochemistry , environmental health
In vitro antigen‐specific proliferation was investigated in a lymphocyte population that had been taken from the peritoneal exudate cells (PEC) of C3H/HeN mice (Ia k ) primed in vivo with both bacterial lipopolysaccharide (LPS) and horse red blood cells (HRBC) and had been purified by passage through a nylon fiber column (Nfc). The proliferative response of the Nfc‐passed lymphocytes primed with HRBC and LPS [T(HRBC + LPS) cells] depended on the dose of antigen in the cultures, and the response was higher than that of cells prepared from mice primed with HRBC alone [T(HRBC) cells]. No response was seen in the cells prepared from the LPS‐primed mice [T(LPS) cells] or normal mice [T(N) cells]. The response of the T(HRBC) cells was abolished by previous treatment of the cells with anti‐Ia k antibody and complement (C), whereas the response of the T(HRBC + LPS) cells was retained after the same treatment, indicating that the Ia – T(HRBC + LPS) cells can proliferate in response to antigen in spite of Ia+ accessory cell‐depletion. Supernatants from the cultures of Ia – T(HRBC + LPS) cells in the presence of HRBC showed abundant IL‐2 activity, while those of Ia – T(HRBC) cells did not. The IL‐2 should be produced by the L3T4 cell population in T(HRBC + LPS) cells in response to antigen, since the previous treatment of the cells with anti‐L3T4 antibody and C abrogated the production. On the other hand, the Ia – T(HRBC + LPS) cells as well as the Ia – T(LPS) cells could respond to IL‐2 dose‐dependently when recombinant IL‐2 was added into the cultures, but the response of Ia – T(HRBC) cells to IL‐2 was very weak. The cell population responding to IL‐2 in the T(HRBC + LPS) cells as well as T(LPS) cells must be AsGM1‐positive or natural killer (NK) cells, since previous treatment of the cells with anti‐AsGM1 antibody and C abrogates the response. Together these results suggest that L3T4 lymphocytes capable of producing IL‐2 in response to HRBC antigen without Ia + accessory cells are generated in the PEC of the mice after priming with LPS and antigen together, and the IL‐2 produced by the L3T4 lymphocytes induces the proliferation of the LPS‐primed AsGM1+ cells.