By Henry G. Kunkel, Frank J. Dixon (Eds.)
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Extra info for Advances in Immunology, Vol. 33
W39) could block the T-cell proliferative responses induced in H-2b mice by beef insulin (Rosenwasser and Huber, 1981). , 1977; 30 IRWIN SCHEH 0 1 2 3 4 6 0 1 2 3 4 6 NO. 6. Comparison of the antigen-presenting accessory cell function of SAC from normal male (DBA/2 x CBA/N)F, ( 0 )or abnormal male (CBA/N x DBA/2)F1mice (A) pulsed with TNP-KLH (open figures, A), TNP-Ficoll (open figures, B), or medium (closed figures, A and B). , 1980). W39 is expressed by these cells and is important for the presentation of beef insulin to T cells.
1980). These studies suggested that the shift to the K predominant phenotype occurred in normal mice at 4 to 6 weeks of age, in apparent coincidence with the development of large numbers of p+6+ B cells. , 1980). In addition, in a double-blind study of F, mice (F, x Fl), the low K / A ratio was associated with an inability of these mice to respond to TI-2 antigens or to form B-cell colonies in soft agar. The results of these studies are distinct from those obtained in two n 3 60- Y LL 48 - AGE OF MICE IN DAYS FIG.
Furthermore, treatment with antimouse thymocyte serum reduced the polyclonal response of F, female spleen cells to LPS, but did not alter the F, male response. Thus, while there appears to be subtle abnormalities in the T-cell function of CBA/N immune-defective mice, these cannot explain the abnormalities in their T D antibody responses. , 1975a). Furthermore, although it has been suggested that T cells play an important role in the responses of mice in uitro to the TI-2 antigen TNP-Ficoll, the demonstration that splenic T cell-depleted populations of normal F, female cells will reconstitute TNP-Ficoll responses in defective F, male mice (see Section V1,A) suggests that T cells do not play a primary role in the cellular mechanism(s) underlying the CBA/N immune defect.
Advances in Immunology, Vol. 33 by Henry G. Kunkel, Frank J. Dixon (Eds.)