Lymphocyte subpopulations in primary immunodeficiency disorders

Gupta, Sudhir

doi:10.1007/bf02834434

Cited by 4 publications

(4 citation statements)

References 48 publications

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“…Patients with common variable immu nodeficiency (CVI) are characterized by the presence of low levels of serum immuno globulins, low or normal numbers of circu lating B lymphocytes and, in a subgroup of patients, impairment of cell-mediated im mune response as well [18,25,41], Patients with CVI have imbalance of OKTJ/OKTg T cell subset proportions and abnormal immunoregulatory functions, and they are sus ceptible to increased frequency of autoim mune phenomena [39,62,100,132], Recent ly, we examined AMLR in 18 patients with CVI and compared it with AMLR in 20 ageand sex-matched controls [55a,b], AMLR was decreased in 10 of the 18 patients with CVI. There was no difference in the time kinetics of peak proliferative response, but…”

Section: Primary Immunodeficiencymentioning

confidence: 99%

Autologous Mixed Lymphocyte Reaction in Health and Disease States in Man

Gupta¹

1983

Vox Sanguinis

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In this review are discussed the nature of T cell subsets, defined with monoclonal antibodies, responding in T-non-T and T-T autologous mixed-lymphocyte reactions (AMLR) and antigens stimulating in AMLR, soluble products of AMLR and generation of suppressor, helper and cytotoxic functions. On the basis of these data a model of immunoregulation in vivo can be proposed. We believe that AMLR is a real phenomenon and not an artefact and perhaps represents a mechanism by which various immune functions are regulated, including feedback regulation of AMLR. The significance of AMLR is further supported by studies in various human and animal diseases.

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Section: Primary Immunodeficiencymentioning

confidence: 99%

Autologous Mixed Lymphocyte Reaction in Health and Disease States in Man

Gupta¹

1983

Vox Sanguinis

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“…tumor inoculation renders this model very close to human B-cell lymphoma and CLL. However, in contrast to the rapidly progressive and disseminated disease seen in our xenograft models, human B-cell CLL shows a characteristic stability in the carly stagc of the disease and CLL B cells have been postulated to represent an early phase in tumor progression (Gupta and Good, 1980). The aggressive growth of Dlo.l cells in our xenograft models may be the result of EBV-stimulated progression of the transformed CLL B cclls (Lee et al, 1986) and/or attenuated host resistance in the immunodeficient mice.…”

Section: Discussionmentioning

confidence: 62%

Inhibition of human B‐cell chronic lymphocytic leukemia by a monoclonal antibody in xenograft models

Zhu

Ghose

Lee

et al. 1994

Intl Journal of Cancer

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To establish xenograft models of human B-cell chronic lymphocytic leukemia (CLL), we inoculated 5 x 10(6) D10-1 cells, a subline of Epstein-Barr virus (EBV)-transformed human B-cell CLL with a marker chromosomal anomaly, into SCID or irradiated nude mice by the intravenous (i.v.) or intraperitoneal (i.p.) route. All i.p. tumor-inoculated mice developed rapidly progressive, lethal ascites tumor, and 100% of i.v. tumor-inoculated mice developed disseminated CLL. All mice died of tumor within 8 weeks of tumor inoculation. Tumor-inoculated SCID mice died earlier with wider tumor dissemination than the tumor-inoculated nude mice. All the tumor-inoculated mice had histologically confirmed metastases in lymph nodes, and most of them also had metastases in one or more internal organs. Cytogenetic analysis confirmed the origin of these tumors from the xenografted D10-1 cells. The D10-1 cells harvested from the xenografts did not differ from the parent D10-1 cells as regards (i) reactivity with 2 monoclonal antibodies (MAbs) directed against CLL-associated cell-surface antigens; (ii) rate of proliferation in vitro; and (iii) sensitivity to the 2 chemotherapeutic agents, methotrexate and adriamycin. Administration of 50 micrograms/mouse of Dal B02, an IgG1 (kappa) MAb directed against surface-associated antigens of human B-cell CLL, significantly prolonged the survival of D10-1-inoculated nude and SCID mice. The MAb was more effective in D10-1-inoculated nude mice than in SCID mice. In all the D10-1 xenograft models, the effectiveness of Dal B02 decreased with higher tumor load but increased with the amount of MAb injected. Dal B02 F(ab)'2 fragment failed to demonstrate any anti-tumor activity in D10-1-inoculated nude mice. In vitro assays revealed that Dal B02 had no direct inhibitory effect on D10-1 cells, but could be cytotoxic towards D10-1 cells in the presence of splenic cells or peritoneal macrophages from nude and SCID mice, or together with rabbit complement.

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“…predominance of mature macrophages and active haemophagocytosis. Although investigations to exclude an opportunistic viral infection were incomplete in these patients, it is quite likely they had such an infection because of their immunodepressed state; CLL patients frequently have hypogammaglobulinaemia (Gupta & Good 1978), defective natural killer activity, defective antibody associated cytotoxicity (Gupta & Good 1980) and absent serum interferon (Ludwig 1979), and their immunosuppression is increased by previous cytotoxic therapy.…”

Section: Clinical Summary Of Cases With Hmr-like Syndrome Complicatinmentioning

confidence: 99%

Histiocytic Medullary Reticulosis Complicating Chronic Lymphocytic Leukaemia: Malignant or Reactive?

Manoharan

Catovsky

Lampert

et al. 1981

Scandinavian Journal of Haematology

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We describe 4 patients with a haemophagocytic syndrome resembling histiocytic medullary reticulosis (HMR) complicating chronic lymphocytic leukaemia (CLL) of 9 months to 8 years duration. Surface marker studies in 2 cases showed that the CLL lymphocytes were of B-cell type in one and of T-cell type in the other. 2 of the patients had histiological evidence of co-existing immunoblastic sarcoma at the time of diagnosis of the =-like syndrome and all 4 patients died within 3 weeks of this diagnosis. The pathogenesis of the HMR-like syndrome in these patients is discussed and it is concluded that it is probably reactive to an underlying opportunistic viral function related to their immunodepressed state secondary to CLL and/or the cytotoxic therapy.

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Lymphocyte subpopulations in primary immunodeficiency disorders

Cited by 4 publications

References 48 publications

Autologous Mixed Lymphocyte Reaction in Health and Disease States in Man

Autologous Mixed Lymphocyte Reaction in Health and Disease States in Man

Inhibition of human B‐cell chronic lymphocytic leukemia by a monoclonal antibody in xenograft models

Histiocytic Medullary Reticulosis Complicating Chronic Lymphocytic Leukaemia: Malignant or Reactive?

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