The human leucocyte-common (LC) molecule: Dissection of leukaemias using monoclonal antibodies directed against framework and restricted antigenic determinants

Ritter, Mary A.; Sauvage, C A; Pegram, Susan; Myers, Christopher D.; R, Dalchau; Fabre, John W.

doi:10.1016/0145-2126(85)90152-3

Cited by 11 publications

(2 citation statements)

References 19 publications

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“…Mouse anti-human CD45 mAb F10-89-4 and CD45RA mAb F8-11-13 were provided by Rosemarie Dalchau (London, U.K.) (17). Anti-CD45 RO mAb UCHL-1 was provided by P. C. L. Beverley (London, U.K.) (18).…”

Section: Monoclonal Absmentioning

confidence: 99%

Linkage of the CCR5Δ32 Mutation with a Functional Polymorphism of CD45RA

Liao

Montefiori

Patel

et al. 2000

The Journal of Immunology

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A 32-bp deletion in CCR5 (CCR5Δ32) confers to PBMC resistance to HIV-1 isolates that use CCR5 as a coreceptor. To study this mutation in T cell development, we have screened 571 human thymus tissues for the mutation. We identified 72 thymuses (12.6%) that were heterozygous and 2 (0.35%) that were homozygous for the CCR5Δ32 mutation. We found that thymocyte development was normal in both CCR5Δ32 heterozygous and homozygous thymuses. In 3% of thymuses we identified a functional polymorphism of CD45RA, in which cortical and medullary thymocytes failed to down-regulate the 200- and 220-kDa CD45RA isoforms during T cell development. Moreover, we found an association of this CD45 functional polymorphism in thymuses with the CCR5Δ32 mutation (p = 0.00258). In vitro HIV-1 infection assays with CCR5-using primary isolates demonstrated that thymocytes with the heterozygous CCR5Δ32 mutation produced less p24 than did CCR5 wild-type thymocytes. However, the functional CD45RA polymorphism did not alter the susceptibility of thymocytes to HIV-1 infection. Taken together, these data demonstrate association of the CCR5Δ32 mutation with a polymorphism in an as yet unknown gene that is responsible for the ability to down-regulate the expression of high m.w. CD45RA isoforms. Although the presence of the CCR5Δ32 mutation down-regulates HIV-1 infection of thymocytes, the functional CD45RA polymorphism does not alter the susceptibility of thymocytes to HIV-1 infection in vitro.

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Section: Monoclonal Absmentioning

confidence: 99%

Linkage of the CCR5Δ32 Mutation with a Functional Polymorphism of CD45RA

Liao

Montefiori

Patel

et al. 2000

The Journal of Immunology

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“…For immunoblots, the antibody concentration was 10 μg/ml. We also used mouse anti-human Thy-1 mAb, clone F15-42-01 [48] (Dr. Rosemarie Dalchau, Institute of Child Health, London, UK), a marker of placental decidual cells (and fibroblasts and brain tissue) [46], mouse anti-rat Thy-1, clone OX-7 [49] (Dr Alan F. Williams, University of Oxford, Oxford, UK), mAbs against CD68, a marker of tissue macrophages, and CD14, a marker of monocytes (Dako Corporation, Carpinteria, CA), and leukocyte-common antigen, clone F10-89-4 [50] (Dr. John F. Fabre, Institute of Child Health, London, UK).…”

Section: Methodsmentioning

confidence: 99%

Multiple luteinizing hormone receptor (LHR) protein variants, interspecies reactivity of anti-LHR mAb clone 3B5, subcellular localization of LHR in human placenta, pelvic floor and brain, and possible role for LHR in the development of abnormal pregnancy, pelvic floor disorders and Alzheimer's disease

Bukovský

Indrapichate

Fujiwara

et al. 2003

Reprod Biol Endocrinol

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Distinct luteinizing hormone receptor (LHR) protein variants exist due to the posttranslational modifications. Besides ovaries, LHR immunoreactivity (LHRI) was also found in other tissues, such as the brain, fallopian tube, endometrium, trophoblast and resident tissue macrophages. The 3B5 mouse monoclonal antibody was raised against purified rat LHR. In rat, porcine and human ovaries, the 3B5 identified six distinct LHR bands migrating at ~92, 80, 68, 59, 52 and 48 kDa. Characteristic LHRI was detected in rat, human and porcine corpora lutea. During cellular differentiation, subcellular LHR distribution changed from none to granular cytoplasmic, perinuclear, surface, nuclear and no staining. There were also differences in vascular LHR expression – lack of LHRI in ovarian vessels and strong staining of vessels in other tissues investigated. In normal human term placentae, villous LHRI was associated with blood sinusoids and cytotrophoblast cells, and rarely detected in trophoblastic syncytium. In all abnormal placentae, the LHRI of sinusoids was absent, and syncytium showed either enhanced (immature placental phenotypes) or no LHRI (aged placental phenotype). LHRI in human brain was identified in microglial cells (CD68+ resident macrophages). Protein extracts from human vaginal wall and levator ani muscle and fascia showed strong ~92 and 68 kDa species, and LHRI was detected in smooth muscle cells, fibroblasts, resident macrophages and nuclei of skeletal muscle fibers. Our observations indicate that, in contrast to the theory on the role of vascular hormone receptors in preferential pick up of circulating hormones, there is no need to enhance selective pick up rather only prevent LH/CG transport to inappropriate sites. Abnormal placental LHR expression may play a role in the development of abnormal pregnancy. Expression of LHR in the pelvic floor compartments suggests that high LH levels in postmenopausal women may contribute to the pelvic floor relaxation and increased incidence of pelvic floor disorders. Since chorionic gonadotropin increases secretion of a variety of cytokines by monocytes, and induces their inflammatory reaction and phagocytic activity, high LH levels in aging individuals may also activate microglia (mononuclear phagocyte system in the central nervous system) and contribute to the development of Alzheimer's disease and other inflammation-mediated neurodegenerative diseases.

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Cell Surface Markers in Leukemia and Lymphoma

Freedman

1991

Blood Cell Biochemistry

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The human leucocyte-common (LC) molecule: Dissection of leukaemias using monoclonal antibodies directed against framework and restricted antigenic determinants

Cited by 11 publications

References 19 publications

Linkage of the CCR5Δ32 Mutation with a Functional Polymorphism of CD45RA

Linkage of the CCR5Δ32 Mutation with a Functional Polymorphism of CD45RA

Cell Surface Markers in Leukemia and Lymphoma

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