Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Jerrold Schwaber is active.

Publication


Featured researches published by Jerrold Schwaber.


The New England Journal of Medicine | 1981

Deficiency of T Helper Cells in Transient Hypogammaglobulinemia of Infancy

R. Lawrence Siegel; Thomas Issekutz; Jerrold Schwaber; Fred S. Rosen; Raif S. Geha

We studied 17 patients with transient hypogammaglobulinemia of infancy to define the immunologic defect responsible for this disorder. The number of circulating B cells in these patients was normal, as was the ability of the B cells to synthesize immunoglobulins when stimulated with Epstein-Barr virus, a direct B-cell activator. However, the capacity of the B cells to synthesize IgG in response to pokeweed mitogen, a T-cell-dependent B-cell activator, was depressed. Experiments with cultured lymphocytes indicated that excess suppressor-cell activity was not present in these patients, but that their T cells were deficient in providing help to B cells from their normal parents. A numerical deficiency in T4-positive (T4+) helper cells was found. Patients who had recovered from the disorder had a normal number of T4+ helper cells. Our results indicate that a numerical, as well as a functional, deficiency in helper T cells underlies the deficiency in IgG production in transient hypogammaglobulinemia of infancy.


Clinical Immunology and Immunopathology | 1983

Frequency of anti-DNA antibody producing cells from normals and patients with systemic lupus erythematosus

Susan Hoch; Peter H. Schur; Jerrold Schwaber

The frequency of anti-DNA antibody producing cells from normals and patients with systemic lupus erythematosus (SLE) was determined. Peripheral blood lymphocytes (PBL) from normals and patients with SLE were cultured for 8 and 15 days with and without transformation by Epstein-Barr virus (EBV). Culture supernatants were examined for the presence of anti-DNA antibody using an enzyme-linked immunosorbent assay. We found that PBL from patients with SLE spontaneously produce anti-DNA antibodies whereas PBL from normals do not. After EBV transformation, anti-DNA antibody producing cells were detected in both cultures from patients with SLE as well as from normals. These data suggest that the high levels of anti-DNA antibody observed in patients with SLE represent activation of B cells committed to anti-DNA antibody production and that such cells are present but are not activated in normal individuals.


Cell | 1977

Abelson virus-transformed lymphocytes: Null cells that modulate H-2

Diane McMahon Pratt; Jack L. Strominger; Robertson Parkman; David L. Kaplan; Jerrold Schwaber; Naomi Rosenberg; Charles D. Scher

A-MuLV-transformed lymphoid cells from Balb/c mice had the properties of null lymphocytes. They did not secrete Ig and all but one did not have detectable cell-associated Ig; one line synthesized, but did not secrete, the mu chain of IgM. The cells expressed H-2D and H-2K, but not H-21 histocompatibility antigens or theta-antigen; they had Fc receptors. Most cell lines grew to form donor cell tumors after inoculation into (Balb/c X C57B1/6)F1 mice. The tumor cells have more H-2Dd than cells passaged in vitro. Cell lines carried in vitro progressively lost H-2Dd. A line in which 5-30% of the cells were lysable by anti-H-2Dd was cloned; all eleven clones had H-2Dd (13-69% lysable) demonstrating that H-2 modulates in vitro. A clone with little H-2Dd (10-15% lysable) was tumorigenic even after treatment with anti-H-2Dd sera; at least 50% of the tumor cells were lysed by anti-H-2Dd. Thus A-MuLV-transformed lymphocytes modulate H-2 in vivo to higher levels and in vitro to lower levels.


Clinical Immunology and Immunopathology | 1981

IgM-restricted production of immunoglobulin by lymphoid cell lines from patients with immunodeficiency with hyper IgM (dysgammaglobulinemia)☆

Jerrold Schwaber; Herbert Lazarus; Fred S. Rosen

Abstract Patients with immunodeficiency with hyper IgM have elevated levels of serum IgM and sometimes IgD, with absent IgG and IgA. To examine the cellular basis of this deficiency, B lymphocytes from five patients with this disease were transformed by Epstein-Barr virus (EBV). The resulting lymphoid cell lines bore surface IgM and IgD, but no IgG or IgA. IgM was secreted by cell lines for all five individuals. No secretion of IgG, IgA, or IgD was detected. The restricted expression of IgM and IgD as surface molecules and secretion of IgM only contrasts with the expression of multiple classes of immunoglobulin by recently established cell lines from normal individuals. These results demonstrate there is a primary B lymphocyte defect responsible for immunodeficiency.


Journal of Clinical Investigation | 1988

Correction of the molecular defect in B lymphocytes from X-linked agammaglobulinemia by cell fusion.

Jerrold Schwaber; Nathan Koenig; John Girard

The X chromosome-linked antibody deficiency disease, X-linked agammaglobulinemia (XLA), results from failure of B lymphoid development. In the minor form of XLA, B lymphoid development terminates at the stage of immature B lymphocytes that produce truncated Ig heavy (H) chains composed of D-J-C(mu/delta), resulting from failure of VH gene rearrangement. Fusion of B cells from a patient with the minor form of XLA with mouse myeloma results in complementation of this defect; hybrid cells produce full-length H chains composed of VH-D-JH-C. The VH gene is of human origin. Complementation occurs independent of retention or loss of the human X (XLA) chromosome in the hybrid cells. These results indicate that the D-JH-C structure of the XLA B cells is fully functional for the subsequent rearrangement of a VH gene element, and that failure of immunoglobulin expression is susceptible to correction.


Cellular Immunology | 1982

Improved method for cloning human B-cell lines

Susan Hoch; Peter H. Schur; Jerrold Schwaber

Abstract Difficulties in the successful cloning of B-cell lines have prevented widespread establishment of specific antibody-forming human B-cell lines. We have improved on standard methods of cloning by culturing human lymphoid cells suspended in agarose with nonproliferating human fetal lung fibroblasts. Using this method, cloning efficiencies up to 20% were observed, from as few as 50 plated lymphoid cells. These results are significantly better than the efficiencies of up to 1% using 5 to 10 × 10 3 cells with traditional soft agar methods. The number of colonies observed increased in proportion to the number of fibroblasts plated with the lymphoid cells. A threshold number of fibroblasts was found. Microscopically, close association between lymphoid cells and fibroblasts was seen. A growth-enhancing factor appears to be produced by fibroblasts suspended in agarose. This cloning method is applicable to both well-established and newly established lymphoid cell lines and should be useful for growing and cloning B cells.


Journal of Clinical Investigation | 1992

Evidence for Failure of V(D)J Recombination in Bone Marrow Pre-B cells from X-linked Agammaglobulinemia

Jerrold Schwaber

X-linked agammaglobulinemia (XLA) results from a failure of B lymphoid development. We have previously examined pre-B cell hybrids from three patients with XLA and found them to be limited to production of a novel germ line transcript of the Ig H chain locus composed of a leader sequence (LS) spliced to the constant region of mu chain (C mu) as mRNA and polypeptide. These transcripts result from transcriptional activation of the germ line heavy chain locus from an LS exon upstream of the embryonic JH locus. Germ line LS-C mu transcripts are produced by pre-B cells from normal bone marrow and fetal liver, indicating that they are products of normal pre-B cell development, as part of the process of transcriptional activation to provide access for the recombinase. Bone marrow from three patients with XLA has been examined directly by polymerase chain reaction amplification to determine whether the exclusive production of LS-C mu by XLA pre-B cell hybrids is representative of XLA pre-B cells. I report that LS-C mu is the predominant Ig molecule produced by XLA pre-B cells, with limited production of the D mu product of DJH intermediate stage of V(D)J recombination. Mature VHDJH recombinations were not detected with a variety of primers that amplify VH sequences. I conclude that XLA is associated with a limitation in V(D)J recombination that may cause the failure of pre-B cell development.


Journal of Clinical Investigation | 1988

B lymphocytes from X-linked agammaglobulinemia. Delayed expression of light chain and demonstration of Lyonization in carriers.

Jerrold Schwaber; Jennifer Payne; Ray Jade Chen

We report an unusual phenotype of B cells in a patient with X-linked agammaglobulinemia (XLA), and cellular evidence for Lyonization of B cells from his mother and sister. The patient has a failure of B cell maturation at the stage of early B lymphocytes, associated with production of D(mu delta) H chain. The phenotype of his B cells includes: (a) limitation to expression of the mu and delta H chain isotypes, (b) production of mu and delta H chains of reduced size and (c) delayed expression of L chain. Peripheral blood and B cell lines from the patients mother and sister include 50% cells that express H chain without L chain. B cell lines from the mother and sister produce full-length mu and gamma H chains and truncated mu and delta chains corresponding to the H chains produced by the patients B cells. Clones with normal and XLA phenotype have been isolated from B cell lines derived from the patients mother. We conclude that the dimorphism of mothers and sisters B cells results from Lyonization, implying that the gene defect in XLA is intrinsic to B lymphocytes.


Journal of Clinical Immunology | 1982

Isotypes of surface immunoglobulin on B lymphocytes from patients with immune deficiency.

Jerrold Schwaber; Fred S. Rosen

Peripheral blood lymphocytes from patients with antibody deficiency diseases (primarily agammaglobulinemia) were examined for the presence of B-lymphocyte subsets defined by surface immunoglobulin isotypes. The patients could be classified into one of four groups based upon the presence or absence of particular isotype-defined subsets. Patients with type I agammaglobulinemia lacked cells bearing surface IgG as well as IgD− Igm+-bearing cells. Type II agammaglobulinemia had unusually large numbers of IgG-bearing cells, representing as many as 50% of the peripheral blood B lymphocytes, while other B-cell subsets were present in normal numbers. Type III agammaglobulinemia had apparently normal numbers of all B-cell subsets. Hyper IgM immunodeficiency lacked cells bearing surface IgG, but did have all three IgD/IgM-bearing B-cell subsets. This classification of patients based upon B-cell subsets present in peripheral blood directly correlates with previous functional studies of B cells from these patients. We suggest that abnormalin vitro function of cells from these patients results from abnormal populations of B cells in peripheral blood, which result from the underlying disease.


Human Mutation | 2000

BTK mutations in patients with X-linked agammaglobulinemia: Lack of correlation between presence of peripheral B lymphocytes and specific mutations Communicated by: Mark H. Paalman Online Citation: Human Mutation, Mutation in Brief #377 (2000) Online http://journals.wiley.com/1059-7794/pdf/mutation/377.pdf

Luan Tao; Mark T. Boyd; Greg Gonye; Barbara Malone; Jerrold Schwaber

X-linked agammaglobulinemia (XLA) is a human antibody deficiency that results from mutation of the tyrosine kinase btk. We tested the hypothesis that XLA patients who varied from the classic phenotype of XLA by presence of normal or near normal number of peripheral B lymphocytes would have a set of mutations of BTK that is different from the mutations found in patients without peripheral B lymphocytes. The mutations of BTK we found in two patients with normal numbers of peripheral B lymphocytes have been previously identified in patients without peripheral B lymphocytes. A third patient, without peripheral B cells, was found to express normal levels of wild type btk. Exmination of the mutations of the BTK gene in patients in the BTKbase who were identified as having peripheral B lymphocytes found that these same mutations, or mutations of the same protein domains, were also present in patients identified as lacking peripheral B lymphocytes. Analysis of mutations in BTK has previously led to the conclusion that severity of disease in XLA cannot be predicted from the specific mutation of BTK. The results of this study suggest that whether an XLA patient will develop peripheral B lymphocytes cannot be predicted from the specific mutation of BTK.

Collaboration


Dive into the Jerrold Schwaber's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Naomi Rosenberg

Massachusetts Institute of Technology

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Peter H. Schur

Brigham and Women's Hospital

View shared research outputs
Researchain Logo
Decentralizing Knowledge