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Biomedical subjects

L J Greenberg

Publications and source records attributed to L J Greenberg.

At least 19 recordsLinked to original sources
PubMed1991

Genetic linkage between Huntington disease and the D4S10 locus in South African families: further evidence against non-allelic heterogeneity.

A study of genetic linkage between Huntington disease (HD) and the D4S10 locus (G8) has been undertaken in 10 South African (SA) families originating from the black, white and mixed acestry population groups. Allele frequencies at the D4S10 locus have been established in the non-Caucasoid population groups. There are significant differences in the allele frequencies at the D4S10 locus between the various SA populations. Clearly, information about population-specific frequencies for all polymorphisms is essential prior to the implementation of predictive testing in different population groups. Linkage has been demonstrated within this mixed group of HD families in SA using the HindIII, EcoRI and MspI polymorphisms, detected by G8. A maximum lod score of 8.14 at a recombination fraction of 0.00 (confidence limit 0-0.058) has been calculated using a combined haplotype of the HindIII and MspI polymorphisms. Taking into account the diverse ethnic backgrounds of the different SA population groups in this investigation, the data obtained from the study provide further evidence that there is probably only a single HD locus.

Alleles↗
PubMed1990

Tumor marker kinetics in the monitoring of breast cancer.

Controversy exists in using carcinoembryonic antigen (CEA) for monitoring the clinical course of breast cancer. In this study, the kinetics of two plasma tumor markers, CEA and CA15-3, immediately after the initiation of chemotherapy were assessed in 30 patients with advanced breast cancer. Four distinct kinetic patterns were seen. Two patterns fitted the expected relationship where the plasma marker increased during tumor progression (nine patients), and declined in tumor regression (five patients). The third pattern was paradoxical in that objective tumor regression in eight patients was associated with an acute surge of these markers followed by a steady decline. The doubling times for both CEA and CA15-3 were immediately shortened four-fold after therapy suggesting tumor cytolysis in treatment responders. Equally paradoxical was the fourth pattern where tumor progression in eight patients was associated with a rapid and transient decline of markers followed by rebounds. Such a rapid decline may be due to a suppression of marker release, as demonstrated in an in vitro study. Adequate knowledge of these putative paradoxical patterns will permit their effective use in monitoring the disease course and perhaps in the early prediction of the therapeutic response.

Adult↗
PubMed1979

Anomalous mixed lymphocyte culture reactivity between HLA--A, --B, --C, --DR identical siblings.

Complete HLA typing including HLA--A, --B, --C, --DR (D related B cell typing), --D, mixed lymphocyte culture (MLC), and primed lymphocyte testing (PLT), together with complete red blood cell (RBC), glyoxalase (GLO), GBG (Factor B), and phosphoglucomutase 3 (PGM3) typings were performed on a informative family. The five siblings inherited the four possible combinations of parental HLA haplotypes, and two of the siblings were HLA--A, --B, --C and --DR identical. Repeated MLC testing of the family revealed positive mixed lymphocyte reactivity in all combinations. B cell typing for the DR specificities demonstrated no variation from the expected inheritance pattern and specifically no recombination event. GBG and GLO typings militated against a recombination involving the paternal chromosome. HLA--D testing revealed that only one of the HLA--A, --B, --C, and --DR identical siblings gave typing responses to the HLA--Dw3 specificity present on that maternal haplotype. Utilizing HLA haploidentical combinations, lymphocytes were primed against the four parental haplotypes and the non-Dw3 haplotype of interest (Aw24--B8--DRw3--LDY) in the PLT. The sibling inheriting this haplo-type did not restimulate cells primed against the A2--B40--DRW6--LDY specificity. Furthermore, no discrimination was observed in the restimulation of lymphocytes primed against this haplo-type. Possible interpretations of these family data include: a spontaneous mutation, non-major histocompatibility locus (MHC) stimulation, and HLA--DR/D recombination.

B-Lymphocytes↗
PubMed1978

Serological inhibition of blast transformation to purified streptococcal antigens by planned immunization in HLA (A,B) compatible unrelated individuals.

Sera obtained from planned immunizations between unrelated donors and recipients, identical or compatible at HLA-A and B, were assessed for their capacity to alter the in vitro response of a test panel of lymphocytes to PHA and a purified streptococcal antigen (PAS). In the case of PHA, no serum effects were apparent. The response to PAS, however, significantly inhibited by two sera. When tested for their complement-dependent cytotoxicity on enriched populations of T and B lymphocytes, none of the sera manifested cytotoxicity against T cells nor did serological inhibition correlate with the capacity to lyze B cells. The data suggest that inhibition of the PSA response is mediated by blocking antibodies specific for a subset of lymphocytes, possibly T cells. While the precise mechanism governing the response to PSA is not known, the data are compatible with the idea that an HLA-linked Ir gene, expressed on a subset of T lymphocytes, controls immune responsiveness to PSA.

Antibody Specificity↗
PubMed1977

Previously unexplained HLA antigens of combined immunodeficiency disease due to Ia alloantigens.

The presence of extra reactions in the HLA typing of a combined immunodeficiency patient may be attributed to B-cell alloantibodies in the HLA typing sera. The presence of these reactions can be used to identify HLA sera containing B-cell antibodies for further B-cell studies. The alloantibodies in this study have some association with the HLA-D determinants and segregate with HLA in normal families.

B-Lymphocytes↗
PubMed1977

Depressed immune function in epidermodysplasia verruciformis.

Epidermodysplasia verruciformis (EV) is a rare disease characterized by the early onset and unremitting progression of wart-like lesions and frequent association of cutaneous carcinomas. We report two siblings with EV. Immunologic study of both patients demonstrated normal immunoglobulin levels, normal numbers of T-lymphocytes and B-lymphocytes, but markedly depressed in vitro blastogenic reactivity to mitogens and antigens. Cutaneous anergy to a variety of common skin test antigens was noted. These observations may reflect an inherited abnormality in immune function, or the depressed immune function may result from the viral infection of EV.

Adult↗
PubMed1976

Tumor immunology, autoimmunity and aging.

Cell-mediated immune function declines with aging, and may be associated with autoimmunity and malignancy. Humoral immune responses also decline with aging. The chief age-related effect on the immune system is a decrease in T-cell function. The "thymus clock" and immunogenesis are discussed in relation to aging. In animals, attempts at immunologic rejuvenation by cellular or hormonal means have not been successful as the results attained by genetic manipulation.

Aging↗
PubMed1975

Association of HL-A 5 and immune responsiveness in vitro to streptococcal antigens.

Lymphocytes, from randomly selected individuals having normal immune function, when incubated in vitro with varying concentrations of streptococcal antigens, responded in three ways: (a) response over the entire antigen concentration range, i.e., responders; (b) low response to only the highest antigen concentrations; and (c) no response at any antigen concentration. Frequency distribution analysis of these groups indicated that a significant association occurred between the ability to respond and HL-A 5.

Adult↗
PubMed1975

Genetic analysis of patients with chronic active hepatitis.

21 patients with chronic active hapatitis (CAH) and their families were HL-A typed. HL-A8 was significantly increased in frequency. An apparent increased frequency of HL-A1 was shown to be secondary to the increased HL-A8 due to linkage disequilibrium. Genotype analysis revealed a striking increased frequency of homozygosity for HL-A8, 6 of 21 patients (28.5%) vs. 2.8% of controls. Two patients and one normal who were homozygous for both HL-A1 and HL-A8 were found to be homozygous for a mixed lymphocyte culture (MLC) determinant 8a. Homozygous 8a cells were used as test-stimulating cells in one-way MLC reactions to determine the frequency of the expression of the 8a determinant in 17 patients and 49 controls selected for HL-A type. 8a was found to be associated with 50% of HL-A8 haplotypes and was frequent in the patient and control populations of the same HL-A types. These data suggest that susceptibility to CAH is determined by homozygosity for a gene that is in linkage disequilibrium with HL-A8 and more closely associated with the HL-A second locus then with the locus for the major MLC determinant.

Adolescent↗
PubMed1975

Immune deficiency, autoimmunity and aging.

Immune deficiency states in man and animals have been observed at all ages---in the very young, in adult life and the very old. At all ages there appears to be a correlation between immune deficiency and propensity to produce autoantibodies and malignancy. Cellular replacement in immunologically deficient mice results in correction of immune function and slightly increased survival while selected hybridization produces dramatic increases in survival and a delayed onset of autoimmune symptoms. Aging is defined in terms of primary and secondary events where a hypothetic rate of decline of function, called optimum functional longevity, is arbitrarily assigned to the long-lived population. Optimal functional longevity is genetically based and controlled by a hypothetic longevity homeostasis gene complex which includes Ir genes and genes that control endocrine balance.

Aging↗
PubMed1975

Immunodepression after major surgery in normal patients.

Multiple parameters of in vivo and in vitro immune function were measured serially before, during, and following nephrectomy in 12 normal renal transplant donors. All in vitro functions studied (total blood lymphocyte count, B-cell count, T-cell count, mitogen blastogenic response, and mixed leukocyte reactivity as both responder and stimulator) decreased on induction of anethesia and continued to fall during and after operation to reach a low point on the evening after nephrectomy. Depth of depression and rate of recovery varied with the individual function, but all were near normal by the fifth postoperative day. The in vivo delayed hypersensitivity response to cutaneously administered recall antigens declined more gradually and was still falling at the fifth postoperative day. Return of preoperative skin response was delayed, being complete for streptokinase/streptodornase (SK/SD) by 10 to 14 days but incomplete as long as 2 to 3 weeks for mumps and Candida antigens. Serum immunoglobulins did not change. These findings suggest incomplete correlation among the responses to the commonly used in vitro assays of cellular immunity and poor correlation with the in vivo tests. Although surgery and anesthesia results in measurable depression of immune response, clinically significant problems did not arise in these patients.

Adolescent↗