TY - JOUR KW - Animals KW - Antibodies, Bacterial KW - Antibodies, Monoclonal KW - Bacterial Vaccines KW - Hypersensitivity, Delayed KW - Immunization KW - Immunotherapy, Adoptive KW - Lymphocyte Activation KW - Major Histocompatibility Complex KW - Mice KW - Mice, Inbred BALB C KW - Mice, Inbred C57BL KW - Mice, Inbred CBA KW - Mycobacterium KW - Spleen KW - T-Lymphocytes KW - T-Lymphocytes, Helper-Inducer KW - T-Lymphocytes, Regulatory AU - Shroff K E AU - Sainis K B AU - Sengupta S R AU - Kamat R S AB -

In earlier work, intraperitoneal (i.p.) immunization with Mycobacterium vaccae was shown to generate a T-suppressor (Ts) response but intradermal (i.d.) immunization did not. We have now studied the major histocompatibility complex (MHC) restriction of this Ts response. The ability of C57BL/6 (H-2b), BALB/c (H-2d), and the (C57BL/6 x BALB/c) F1 mice to generate suppression after i.p. immunization with 10(8) killed M. vaccae was investigated. The BALB/c and the F1 mice generated suppression, but the C57BL/6 mice failed to do so. The suppression could be ascribed to Lyt-2+, L3T4- antigen-specific T cells. The F1 suppressors generated after i.p. immunization could suppress the generation of T-cell responses to i.d. immunization with M. vaccae in the parental BALB/c but not in the C57BL/6 mice. Monoclonal anti-I-A antibody could suppress the antigen-induced proliferative response of mice primed i.d. with M. vaccae. In contrast, monoclonal anti-I-E antibody enhanced antigen-specific proliferation of spleen cells primed i.p. with M. vaccae. The suppressors generated by i.p. priming of mice with M. vaccae could also suppress the in vitro antigen-induced proliferative response of i.d.-primed spleen cells; the suppression could be blocked by anti-I-E antibody. Thus, the T-cell-mediated suppression in the above experimental model was I-E restricted. The inability of the C57BL/6 mice to generate suppression after i.p. immunization with M. vaccae was ascribed to the lack of I-E expression by mice of H-2b strain.

BT - International journal of leprosy and other mycobacterial diseases : official organ of the International Leprosy Association C1 -

http://www.ncbi.nlm.nih.gov/pubmed/1827647?dopt=Abstract

DA - 1991 Mar IS - 1 J2 - Int. J. Lepr. Other Mycobact. Dis. LA - eng N2 -

In earlier work, intraperitoneal (i.p.) immunization with Mycobacterium vaccae was shown to generate a T-suppressor (Ts) response but intradermal (i.d.) immunization did not. We have now studied the major histocompatibility complex (MHC) restriction of this Ts response. The ability of C57BL/6 (H-2b), BALB/c (H-2d), and the (C57BL/6 x BALB/c) F1 mice to generate suppression after i.p. immunization with 10(8) killed M. vaccae was investigated. The BALB/c and the F1 mice generated suppression, but the C57BL/6 mice failed to do so. The suppression could be ascribed to Lyt-2+, L3T4- antigen-specific T cells. The F1 suppressors generated after i.p. immunization could suppress the generation of T-cell responses to i.d. immunization with M. vaccae in the parental BALB/c but not in the C57BL/6 mice. Monoclonal anti-I-A antibody could suppress the antigen-induced proliferative response of mice primed i.d. with M. vaccae. In contrast, monoclonal anti-I-E antibody enhanced antigen-specific proliferation of spleen cells primed i.p. with M. vaccae. The suppressors generated by i.p. priming of mice with M. vaccae could also suppress the in vitro antigen-induced proliferative response of i.d.-primed spleen cells; the suppression could be blocked by anti-I-E antibody. Thus, the T-cell-mediated suppression in the above experimental model was I-E restricted. The inability of the C57BL/6 mice to generate suppression after i.p. immunization with M. vaccae was ascribed to the lack of I-E expression by mice of H-2b strain.

PY - 1991 SP - 49 EP - 57 T2 - International journal of leprosy and other mycobacterial diseases : official organ of the International Leprosy Association TI - Major histocompatibility complex restriction of T-cell suppression of immune response to mycobacteria. UR - http://ila.ilsl.br/pdfs/v59n1a08.pdf VL - 59 SN - 0148-916X ER -