M. Leonardo Satz

Restriction fragment length polymorphism in HLA class II genes of Latin-American caucasian celiac disease patients

In the present study Latin-American celiac disease patients were analyzed for the frequency of certain HLA class II restriction fragment length polymorphisms in order to investigate whether they exhibited the normal associated alleles or showed unusual class II variants. A DPB/RsaI 4.0-kb fragment that was shown to be significantly increased among North Americans celiac disease patients of the DR3,DQw2 haplotype was found with similar frequency in Latin-American control and celiac disease individuals. A DPA/BglII 3.7-kb fragment previously shown to be increased among British celiac disease patients was also present with similar frequency among Latin-American control and celiac disease individuals. These results show that the frequency of the HLA-DP region-derived restriction fragment length polymorphisms linked to celiac disease differs between Caucasian populations of different ethnic backgrounds (Anglo-Saxon and Latin-American). On the other hand, DNA samples from 13 patients and 14 controls bearing the DR5/DR7 phenotype (which is significantly associated with celiac disease in Latin populations) were investigated for the presence of particular restriction fragment length polymorphisms disproportionally present in celiac disease individuals. No significant differences were found between controls and patients when the DNA was analyzed with 10 different restriction enzymes and probes for DRB, DQA, DQB, and DPB HLA class II sequences.

Complete nucleotide sequence of a genomic clone encoding HLA-B35 isolated from a Caucasian individual of hispanic origin identification of a new variant of HLA-B35

The primary structure of an HLA class I genomic clone isolated from a homozygous HLA-B35 Caucasian individual of hispanic origin was determined. The nucleotide sequence of exons 1, 2, 4, 5, 6, and 7 is identical to that of the HLA-B35 allele of Oriental origin reported previously. Exon 3 differs in only three nucleotides present in a stretch of 23 bp. These changes introduce three amino acid substitutions in residues 109 (Leu----Phe), 114 (Asp----Asn), and 116 (Ser----Tyr), two of which (114 and 116) are located in one of the beta sheets at the bottom of the peptide binding site. The nature of these replacements in this HLA-B35 variant is likely to affect peptide binding and recognition by T lymphocytes. Introns 1, 2, 3, 4, 5, and 6 from this genomic clone are identical to those present in HLA-Bw58, further confirming the evolutionary origin of HLA-B35.

Complete sequence of a new HLA-B35 allele found in a tribe of Mapuche Indians in the south of Argentina

The nucleotide sequence data reported in this paper have been submitted to the GenBank nucleotide sequence database and have been assigned the accession number U17107. The nameB*3509 was officially assigned by the WHO Nomenclature Committee in December 1994

Induction of multifocal lesions of the testis by passive transfer of immune cells.

Spleen cells obtained from Wistar rats bearing a multifocal damage of the testis that had been induced by an antiserum against a non-collagenous fraction of basement membranes, were able to transfer similar testicular lesions into normal recipients. Damage was characterized by multiple foci of seminiferous tubules with different degrees of cell sloughing and a mild interstitial mononuclear cell infiltrate. The incidence of testicular damage in the transferred recipients was 83%, while in the control group of rats transferred with spleen cells from donors that had been injected with normal rabbit serum only 4% of the animals presented mild lesions. In order to determine which lymphocyte subpopulations were effective in transferring the disease, rat spleen cells were treated with murine monoclonal antibodies W3/25 and OX8 or with a rabbit anti-rat IgG serum and complement, before the transfer. A multifocal damage of the testes, indistinguishable from that obtained with the untreated spleen cells was transferred in 50% and 25% of the rats injected with spleen cells depleted in B or in T lymphocytes, respectively. The most severe lesions were observed in the rats transferred with cell populations depleted in B cells.