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Host granulomatous inflammation in murine schistosomiasis mansoni is a T cell-mediated immune response, which, at the chronic stage of the disease, undergoes T suppressor lymphocyte-dependent modulation. In the present study this phenomenon was further analyzed in vitro. Spleen cells of mice undergoing modulation (20 wk of infection) when mixed with spleen cells of animals exhibiting vigorous granulomatous responses (8 wk of infection) abrogated in vitro migration inhibition factor (MIF) production by the latter. Characterization of the delayed-type hypersensitivity T lymphocytes involved in lymphokine production showed that they belonged to the Lyt-1+ subset and did not express I region-encoded antigens. In contrast, T lymphocytes involved in the suppression of MIF activity belonged to the Lyt-2+ subpopulation of cells, which expressed I-J- and I-C-subregion determinants. These results suggest that the modulation of the granulomatous hypersensitivity response in mice is the result of T-T cell interaction with subsequent regulation of inflammatory lymphokine production.

The S region of H-2 controls a polymorphism of the gamma-chain of C4 (gamma 1, gamma 2, and gamma 3) as shown by differences in their isoelectric points. The G region of H-2 was defined by the presence of an alloantigen (H-2.7) on erythrocytes and serum. We found that antisera to H-2.7 immunoprecipitated C4 and no other protein from mouse EDTA-plasma. Furthermore, all H-2.7-positive strains bear C4-gamma 1, and conversely, H-2.7-negative mice bear C4-gamma 2 or gamma 3 (with one exception; see below). The H-2.7 specificity resides on C4d, a 45,000-mol wt fragment generated from the cleavage of the alpha'-chain of C4b by serum control proteins. Because the C4d fragment bears the labile binding site of C4 for cell membranes, it is likely that the erythrocyte alloantigen is acquired from serum as a result of the activation of C4. On the basis of these findings, the existence of a separate G locus is unlikely. Our results also show that C4-gamma 1 and C4-gamma 2 differ from each other at least in their alpha- and gamma-chains, and may represent complex allotypes. No trans effects were observed in F1 hybrids between H-2.7-positive and -negative mice. Mice that bear the k allele in the S region are exceptional in two respects: they are C4-deficient and their C4 molecules bear gamma 2 chains and the H-2.7 alloantigen. Perhaps the low levels of C4 are a consequence of the genetic event leading to this unusual alpha-gamma-chain combination.

A quantitative immunochemical determination of the plasmin inhibitors alpha-1-antitrypsin, alpha-2-macroglobulin, and antithrombin-III of the fibronolytic system was carried out from normal, inflammatorily changed, and essentially sanguineous fluids. The low total inhibitor concentration in the cerebrospinal fluid is due to the 'restricted diffusion' caused by the blood/brain barrier function and the lacking synthesis for these proteins in the central nervous system. The inhibitor concentrations which in functional disorders of the blood/sbrain barrier and/or direct entering of blood are still--low as compared to the plasma produce a dissociation of the plasmin-inhibitor complex. The lacking interaction between the active enzyme and the inhibitor enables the occurrence of a free fibrinolytic activity in the cerebrospinal fluid.