To clarify the immune mechanism in myocarditis, we examined by immunofluorescence techniques the serial changes in percentages of T and B lymphocytes in the heart, spleen, and peripheral blood of DBA/2 mice inoculated with encephalomyocarditis (EMC) virus (experiment I To confirm the involvement of T cells in the development of myocarditis, we also carried out studies in which BALB/c-nu/nu mice (group 1, n = 58), BALBI c-nu/+ mice (group 2, n = 54), and BALB/c-nu/nu mice injected with 5 x 107 spleen cells from BALB/c-nu/ + mice (group 3, n = 50) were inoculated with EMC virus (experiment II). Four mice from each of the three groups were killed on day 6 for virologic studies. In experiment II, there were no significant differences in the incidence of myocarditis among the three groups. Virus titrations of the heart and serum neutralizing antibody titers did not show any significant differences between the three groups on days 6 and 16. Fifty-two percent of group 2 mice (26 of 50) and 43% of those in group 3 (20 of 46) died on days 9 to 15, when congestive heart failure developed. However, only 9% of group 1 (five of 54) died during this period. Pathologic examination confirmed the presence of congestive heart failure in groups 2 and 3 but not in group 1 during this period. Cellular infiltrations and myocardial necrosis were minimal in group 1. Thus, the severity of myocarditis seems to be mediated by T cells. The so-called silent myocarditis seen clinically may be similar to myocarditis in BALB/c-nu/nu mice. Circulation 71, No. 6, 1247-1254, 1985 MYOCARDITIS can develop rapidly and progress to congestive heart failure.' Congestive heart failure has been reported to result from many viral injections in man.2 Thus, a relationship between viral infection and cardiomyopathy has been suggested,3'4 but complete evidence for it is still lacking. Recently we found congestive heart failure after inducing encephalomyocarditis (EMC) virus infections in BALB/c-nu/ + mice5 and have also observed severe myocarditis in DBA/2
Oligomeganephronia (OMN) is a rare, renal hypoplasia, consisting of reduced number of hypertrophied nephrons. This disorder has been considered to be a congenital but not a genetic disease. We describe the first report, to the best of our knowledge, of familial cases of OMN; two male siblings ran rapidly downhill courses and died 11 and 8 days after births, respectively. In addition, the two patients had similar multiple anomalies; microcephaly, prominent glabella, hypertelorism, antimongoloid slant, epicanthal folds, broad nose, cleft lip and palate, downturned mouth, short philtrum, micrognathia, low set ears, hypospadias, and cryptorchism. Although the patients and the parents had normal G‐banded karyotypes, 4p monosomy syndrome is suggested from clinical features. The implications of this are discussed briefly. ACTA PATHOL. JPN. 35: 449–457, 1985.
A large Japanese family in which some members were homozygous or heterozygous for OKT4 epitope deficiency was studied. Homozygotes, heterozygotes, and normal individuals were identified by differences in the number of OKT4 epitopes on the surfaces of lymphocytes. This deficiency was transmitted as an autosomal codominant trait. The internalization of CD4 molecules and the production of IL-2 by lymphocytes of these subjects were examined. The OKT4 epitope was not needed for internalization of CD4 molecules, and IL-2 was produced in the same amounts by these different kinds of subjects. DNA from four clones lacking OKT4 established from four individuals of this family was sequenced. As reported elsewhere for different subjects, a single nucleotide substitution (CGG-->TGG) was found in all four cell lines. The mutation results in arginine being replaced by tryptophan. Analysis showed different hydrophobicity at positions 239 and 240 from the control, probably giving rise to a conformational change in CD4 accounting for lack of reactivity with the OKT4 monoclonal antibody. The incidence of homozygotes in the Japanese population was found to be 0.47% by examination of 1478 random samples, and on the basis of this value, the incidence of heterozygotes was estimated to be 12.8%.
Synthetic peptide vaccines containing a single Th cell epitope identified in the gp70 envelope glycoprotein of Friend murine leukemia helper virus induced potent protective immunity against Friend virus infection. H-2a/b mice immunized by a single s.c. injection of the CFA emulsion containing a peptide that represented the N-terminal gp70 epitope recovered slowly from initial development of splenomegaly, and most did not develop late leukemia, whereas most of the control mice given an injection of CFA alone showed sustained leukemic splenomegaly after the challenge with Friend virus. The mice of the same genetic background immunized with the C-terminal Th cell epitope by a single injection of a separate synthetic peptide eliminated virus-producing cells from the spleen within 12 days after inoculation of Friend virus complex, and did not develop early splenomegaly or polycythemia. H-2a/a mice were not protected by immunization with either one of the two synthetic peptides. Earlier production and more rapid class switching of virus-neutralizing Abs were observed in H-2a/b mice immunized with the peptide vaccines after the challenge with Friend virus, compared with the responses of the control mice. Detailed kinetic and immunohistopathologic analyses suggested that Th cells might be directly involved in the growth inhibition and elimination of virus-infected erythroid precursor cells.
Heterogeneity of V alpha 1+ and V beta 10+ TCR alpha beta-chains, which are predominantly used in anti-FBL-3 CTL clones established in vitro, was investigated at a nucleotide level in FBL-3 tumor-infiltrating lymphocytes (TIL) in vivo. The majority (90%) of V beta 10+ beta-chains dominated in TIL used homogeneous V beta 10D beta 2.1 sequences identical to that used in the T cell clones with cytotoxic functions. The homogeneous TCR beta-chain expression was dominant and found to be about 10% of the total TCR beta-chains in the TIL population, which was a greater than 300-to 900-fold increase than in the regional lymph nodes. This is in good agreement with the in vitro data showing that about 11% CTL clones used the homogeneous V beta 10D beta 2.1+ beta-chain. However, the J beta segment does not seem to contribute greatly to the recognition and selection of this TCR because some of homogeneous VD+ beta-chains were associated with J beta segments other than J beta 2.7 of the CTL clones. The frequency of the V alpha 1J alpha 112-2+ alpha-chain expression of the CTL type was much less (3- to 80-fold increase compared to that of lymph node) and also varied in sample materials, indicating the lower contribution of the alpha-chain for the oligoclonality of the TCR. The results were also confirmed by quantitative PCR and RNase protection assays. This suggests that the dominant expression of the homogeneous TCR beta-chain is due to the expansion of the particular anti-FBL-3 CTL in the tumor in situ. Also, the TCR beta-chain, especially the V beta D beta region, rather than alpha-chain is more important for the recognition and selection of the anti-FBL-3 TIL with cytotoxic functions.
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