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JoséE. Alés-Martínez

Researcher at University of Rochester

Publications -  6
Citations -  298

JoséE. Alés-Martínez is an academic researcher from University of Rochester. The author has contributed to research in topics: B-cell lymphoma & Immune tolerance. The author has an hindex of 5, co-authored 6 publications receiving 296 citations. Previous affiliations of JoséE. Alés-Martínez include University of Alcalá.

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Prostaglandin E2 induces apoptosis in immature normal and malignant B lymphocytes

TL;DR: PGE-secreting cells such as macrophages, which inhabit the B cell microenvironments of lymphoid organs, may eliminate a subset of immature B lymphocytes and may be important in controlling the spread of PGE-sensitive malignant B lymphoma cells.
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Immunoglobulins D and M mediate signals that are qualitatively different in B cells with an immature phenotype.

TL;DR: The results show that the transfected cells retained their exquisite sensitivity to anti-IgM-mediated growth inhibition; however, crosslinking of IgD with anti-delta chain antibody did not inhibit their growth and that mIgD expression per se is not sufficient to change the functional phenotype of immature B cells.
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Lymphoma models for B-cell activation and tolerance

TL;DR: It is suggested that anti-mu-mediated growth arrest is due to the direct or indirect inactivation of an active kinase complex capable of pRB phosphorylation, and its effect on a cyclin:kinase complex that can act on pRB in murine B-lymphoma cells.
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Decreased TcR-CD3+ T cell numbers in healthy aged humans. Evidence that T cell defects are masked by a reciprocal increase of TcR-CD3- CD2+ natural killer cells

TL;DR: It is concluded that the increase in TcR‐CD3−CD2+ NK cells masks the T cell reduction in aged humans by normalizing CD2+ cell frequencies, however, NK cells cannot functionally substitute the thymus‐derived lymphocytes they replace.
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Lymphoma models for B-cell activation and tolerance: IX. Efficient reversal of anti-Ig-mediated growth inhibition by an activated TH2 clone

TL;DR: It is reported that complete protection of B lymphomas from anti-Ig was provided by a type 2 helper cell clone, D10.G4, when these T cells were activated by monoclonal anti-CD3.