Nurse-like cells from bone marrow and synovium of patients with rheumatoid arthritis promote survival and enhance function of human B cells.

Shimaoka, Yasunori; Attrep, Jeanne; Hirano, Toshio; Ishihara, Katsuhiko; Suzuki, Ryuji; Toyosaki, Tomoko; Ochi, Takahiro; Lipsky, Peter E.

doi:10.1172/jci3162

Cited by 101 publications

(109 citation statements)

References 54 publications

(55 reference statements)

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“…Nurse-like cells (NLC) are a subset of stromal cells, distinct from FDC or fibroblasts, that can be cultured out of the bone marrow and synovial tissue of RA patients [43,44]. RA-NLC constitutively express IL-6, IL-8 and granulocyte colony-stimulating factor (GCSF) and upregulate expression of IL-1β and TNFα following co-culture with B cells.…”

Section: Other Synoviocyte Interactions With B Cellsmentioning

confidence: 99%

Synovial biology and T cells in rheumatoid arthritis

2005

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Events that occur in rheumatoid arthritis synovial tissues are responsible for the signs and symptoms of joint inflammation and for the eventual destruction of articular and periarticular structures that lead to joint dysfunction and disability. The three most abundant cell populations in RA synovium are synovial macrophages (type A synoviocytes), synovial fibroblasts (type B synoviocytes) and infiltrating T lymphocytes. Other important cell populations include B lymphocytes, dendritic cells, plasma cells, mast cells and osteoclasts. Our current understanding of rheumatoid arthritis is moving beyond previous concepts that view this disease as the consequence of a specific and focused humoral or cellular autoimmune response to a single autoantigen. Rather, a new view of rheumatoid arthritis is emerging, which seeks to understand this disease as the product of pathologic cell-cell interactions occurring within a unique and defined environment, the synovium. T lymphocytes in rheumatoid arthritis synovium interact closely with dendritic cells, the most potent antigen-presenting cell population in the immune system. T cells also interact with monocytes and macrophages and cytokine-activated T cells may be, especially, suited to trigger production of the important cytokine TNFα by synovial macrophages. Recent evidence also suggests a potent bidirectional interaction between synovial T cells and synovial fibroblasts, which can lead to activation of both cell types. An important role for synovial B lymphocytes has been emphasized recently, both by experimental data and by results of clinical interventions. B cells in synovium can interact with fibroblasts as well as with other cells of the immune system and their potential role as antigen-presenting cells in the joint is as yet underexplored. Rheumatoid arthritis synovium may be one of the most striking examples of pathologic, organ-specific interactions between immune system cells and resident tissue cell populations. This view of rheumatoid arthritis also leads to the prediction that novel approaches to treatment will more logically target the intercellular communication systems that maintain such interactions, rather than attempt to ablate a single cell population.

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Section: Other Synoviocyte Interactions With B Cellsmentioning

confidence: 99%

Synovial biology and T cells in rheumatoid arthritis

2005

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“…A number of mechanisms have been proposed to account for the apparently diminished apoptosis of lymphocytes, including the action of cytokines (6 -17), the presence of inhibitors of apoptosis, such as soluble CD95 and Fas ligand (18,19), and the direct impact of cellto-cell contact (20). Among the cells that appear to be active in blocking lymphocyte apoptosis is a population of stromal cells with the characteristics of thymus and bone marrow nurse cells (21,22). Previous studies documented that these stromal cell lines (SCL) blocked B cell apoptosis in vitro (22).…”

Section: T He Synovial Tissue In Rheumatoid Arthritis (Ra)mentioning

confidence: 99%

Rheumatoid Arthritis Synovial Stromal Cells Inhibit Apoptosis and Up-Regulate Bcl-xL Expression by B Cells in a CD49/CD29-CD106-Dependent Mechanism

Hayashida

Shimaoka

Ochi

et al. 2000

The Journal of Immunology

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Inflammatory sites, such as rheumatoid arthritis (RA) synovial tissue, contain large numbers of activated B cells and plasma cells. However, the mechanisms maintaining B cell viability and promoting their differentiation are not known, but interactions with stromal cells may play a role. To examine this, purified human peripheral B cells were cultured with a stromal cell line (SCL) derived from RA synovial tissue, and the effects on apoptosis and expression of Bcl-2-related proteins were analyzed. As a control, B cells were also cultured with SCL from osteoarthritis synovium or skin fibroblasts. B cells cultured with medium alone underwent spontaneous apoptosis. However, B cells cultured with RA SCL cells exhibited less apoptosis and greater viability. Although SCL from osteoarthritis synovium and skin fibroblasts also rescued B cells from apoptosis, they were less effective than RA SCL. B cell expression of Bcl-xL was markedly increased by RA SCL in a contact-dependent manner, whereas B cell expression of Bcl-2 was unaffected. Protection of B cells from apoptosis and up-regulation of Bcl-xL by RA SCL were both blocked by mAbs to CD106 (VCAM-1), but not CD54 (ICAM-1). Furthermore, cross-linking of CD49d/CD29 (very late Ag-4) on the surface of B cells rescued them from apoptosis and up-regulated Bcl-xL expression. These results indicate that SCL derived from RA synovial tissue play a role in promoting B cell survival by inducing Bcl-xL expression and blocking B cell apoptosis in a CD49d/CD29-CD106-dependent manner.

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“…The effect does not occur with circulating or tonsillar B cells [9]. Like CD38, the CD157 receptor seems to play an especially important role in B lymphocyte development and function [6,40].…”

Section: B Lymphocytesmentioning

confidence: 99%

The metamorphosis of a molecule: from soluble enzyme to the leukocyte receptor CD38

Ferrero

Malavasi

1999

Journal of Leukocyte Biology

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Human CD38 is a 45-kDa type II membrane glycoprotein with an intricate pattern of expression in leukocytes, although evidence is accumulating of its quite widespread expression in cells of nonvascular origin. CD38 is a member of a nascent eukaryotic gene family encoding cytosolic and membrane-bound enzymes whose substrate is NAD, a coenzyme ubiquitously distributed in nature. Functionally, CD38 is an eclectic molecule with the ability not only to catalyze but also to signal, to mobilize calcium, and to adhere to itself, to hyaluronan, and to other ligands. Interaction with CD38 on various leukocyte subpopulations has profound though diverse consequences on their life-span, but these effects seem to be independent of the enzymatic activity of the molecule. CD38 challenges our expectations of a surface molecule and we must sift through its many guises to unmask its true nature. J. Leukoc. Biol. 65: 151-161; 1999.

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Nurse-like cells from bone marrow and synovium of patients with rheumatoid arthritis promote survival and enhance function of human B cells.

Cited by 101 publications

References 54 publications

Synovial biology and T cells in rheumatoid arthritis

Synovial biology and T cells in rheumatoid arthritis

Rheumatoid Arthritis Synovial Stromal Cells Inhibit Apoptosis and Up-Regulate Bcl-xL Expression by B Cells in a CD49/CD29-CD106-Dependent Mechanism

The metamorphosis of a molecule: from soluble enzyme to the leukocyte receptor CD38

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