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Auto‐Delayed‐Type Hypersensitivity Induced in Immunodeficient Mice withModified Self‐Antigens
Author(s) -
TARCIC N.,
BALER R.,
NAOR D.
Publication year - 1984
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.1365-3083.1984.tb01018.x
Subject(s) - lymphoblast , spleen , immunology , splenocyte , antigen , delayed hypersensitivity , microbiology and biotechnology , suppressor , biology , chemistry , medicine , cell culture , genetics , cancer
X‐irradialed (250 rad), cyelophosphamide‐treated or AT x A miceinjected with syngeneic trinitrophenylated spleen cells (TNP‐SC) and footpad challenged with syngencic lymphoblasts generated delayed‐type hypersensitivity (DTH) responses 24, 48 and 72 h after challenge. The syngeneic‐DTH (syn‐DTM) response was mediated by Lyt‐l + cells and suppressed withLyt‐1 + 2 + 3 + , I‐J k+ cells. The suppressorcells were obtained from spleens or thymuses of normal syngeneic mice. Suppressor factor (SF) was extracted or released from Lyt‐l + 2 + 3 + , I‐J k+ cells obtained from normal A mice (but noi fromX‐irradiated A mice). The factor blocked the DTH responses of X‐irradiated mice injected with syngeneic TNP‐SC and challenged with syngeneic lymphoblasts when injected into the mice both at the induction phase and the elicitation phase of the DTH. The factor failed to abrogate allogeneic and xenogeneic DTH. However, allogeneic factor (derived from C57BL/6 mice) abolished the syn‐DTH response of mice injected with syngeneic TNP‐SC and challenged with syngeneic lymphoblasts, The SF was produced by Lyt‐1 + 2 + 3 + , I‐J k+ T cells or by thymocytes. The combined extracted product of Lyt‐l + and Lyt‐2 + cells did not abrogate the syn‐DTH response. Normal spleen cells depleted of phagocytes by a magnetic procedure also produced the SF. These findings indicate, therefore, that suppressive factor (or factors; see Discussion in the accompanying paper, Ref. 17) controls the immunological autoreactivity against syngeneic TNP‐SC.