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M C Gelfand

Publications and source records attributed to M C Gelfand.

72 records · Page 4Linked to original sources
PubMed1974

Ontogeny of B lymphocytes. 3. H-2 linkage of a gene controlling the rate of appearance of complement receptor lymphocytes.

The frequency of lymphocytes bearing complement receptors in the spleens of 2-wk old mice appears to be controlled by two independent genes. The presence of a "high" allele at either locus leads to intermediate or high frequency of CRL at 2 wk of age. One of the genes controlling complement receptor lymphocyte (CRL) frequency (CRL-1) is linked to the H-2 complex. Thus, in progeny of (AKR x DBA/2)F(1) x DBA/2, all mice with a low frequency of CRL at 2 wk of age are homozygous for the H-2 type of the low CRL parent (DBA/2). Furthermore, in the B10 series of congenic mice, CRL frequency at 2 wk of age is similar to the frequency in the donor of the H-2 region. Thus, C57BL/10, B10.BR, and B10-D2 mice are all of the low CRL type while B10.A mice are intermediate in CRL frequency at 2 wk. C57BR and DBA/2, the donors of the H-2 complex of the B10.BR and B10.D2, respectively, are of low CRL type while the A/WySn, the donor of the H-2 complex in the B10.A, is an intermediate CRL strain. Similarly in the A/WySn series of congenic mice, A.CA, A.SW, and A.BY are all low CRL strains while the A/WySn is intermediate. Studies of CRL frequency in mice with recombinant H-2 chromosomes (B10.A(2R), (4R), and (5R); B6/TL(+); and A/TL(-)) indicate that CRL-1 is to the right of the Ss-Slp genes and to the left of Tla.

Age Factors↗
PubMedDate not supplied

Therapeutic studies in NZB/W mice. III. Relationship between renal status and efficacy of immunosuppressive drug therapy.

Female NZB/W mice develop a disease closely resembling human systemic lupus and serve as an animal model for therapeutic studies. Several previous studies have demonstrated the efficacy of different immunosuppressive drug regimens in the therapy of glomerulonephritis in NZB/W mice. After the onset of immune complex deposition, treatment with intermittent high doses of cyclophosphamide or daily low doses of the combination of cyclophosphamide, azathioprine, and methylprednisolone has been effective. The present study was designed to compare such effective regimens in mice early in the course of their renal disease versus mice late in the course of glomerulonephritis. One to three injections of high-dose cyclophosphamide during active immune complex deposition and early histologic changes were significantly effective in prolonging survival, whereas treatment late in the course of glomerulonephritis was less effective. Even more striking was the result of low-dose combination therapy. Daily treatment with cyclophosphamide, azathiprine, and methylprednisolone (C + A + M) effectively prolonged survival when started in mice 5 months old, but was of no benefit when started in those 8 months of age. In a concluding experiment, older mice were selected on the basis of degree of renal disease and studied with regard to proteinuria and survival. Those with mild renal disease responded to daily treatment for 6 months with C + A + M at 1 mg/kg of each drug, whereas those with advanced renal disease at the onset of therapy did not benefit.

Age Factors↗
PubMedDate not supplied

Therapeutic studies in NZB/W mice. IV. Effect of combination drug therapy on immune complex deposition.

Azathioprine, cyclophosphamide, and methylprednisolone given individually to NZB/NZW mice retard the development of autoimmune nephritis and prolong survival in these mice. Administration of the combination of all three drugs is superior to one or two drug regimens. In the present study the kidneys of mice treated with all single, double, and triple drug regimens were compared for the degree of deposition of immunoglobulin and complement. The triple drug regimen significantly reduced overall deposition of immunoglobulin and complement compared with any other regimen. Complement and gamma2 were significantly reduced by triple drug therapy compared with any other regimen. The triple drug regimen reduced gamma1 compared with untreated and double drug treated mice. The single, double, and triple drug regimens significantly reduced gammaM deposition to about the same degree. Deposition of gammaA was not significantly reduced by any regimen. Circulating levels of these immunoglobulin classes were not reduced, a fact suggesting that the reduction in autoimmune nephritis resulting from triple drug therapy is associated with superior reduction in immune complex deposition rather than with generalized, non-specific immunodepression.

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