Characterization of a soluble form of CD58 in synovial fluid of patients with rheumatoid arthritis (RA)

Hoffmann, Jörg; Bayer, Bettina; Zeidler, Henning

doi:10.1046/j.1365-2249.1996.41749.x

Cited by 15 publications

(8 citation statements)

References 27 publications

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“…The CD2/CD58 binding is involved in most T-cell interactions with the other cells and in T-cell activation. Moreover, the binding of CD2/CD58 has significant importance in autoimmune diseases such as RA because it plays a crucial role in lymphocyte recruitment to the inflammatory sites [ 101 , 102 ]. The levels of soluble form of CD58 (sCD58) were found to be significantly reduced in sera and synovial fluid of RA patients in relation to healthy donors and patients with SpA.…”

Section: Chondrocyte Antigens As Potential Targets In Inflammatory Jomentioning

confidence: 99%

Antigenic and immunogenic properties of chondrocytes. Implications for chondrocyte therapeutic transplantation and pathogenesis of inflammatory and degenerative joint diseases

Osiecka-Iwan¹,

Hyc²,

Radomska-Leśniewska³

et al. 2018

cejoi

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In physiological conditions chondrocytes are protected from contact with immunocompetent cells by the extracellular matrix, and transplanted fragments of allogeneic cartilage are not rejected. Cartilage produced by allogeneic chondrocytes, however, evokes the immune response of the recipient and is gradually destroyed. Immunisation by allogeneic chondrocytes is induced by the contact of their surface molecules with cells of the immune system. Chondrocytes constitutively express class I and, in some species, class II major histocompatibility complex (MHC) molecules. Expression of MHC class II molecules is induced in vitro by pro-inflammatory cytokines and in vivo in the course of the rejection of transplanted allogeneic cartilage. Low level of MHC class II molecules is found on the surface of human articular chondrocytes in patients with rheumatoid arthritis and osteoarthritis. Cartilage produced by transplanted allogeneic chondrocytes is destroyed by monocytes/macrophages and cytotoxic T and natural killer (NK) cells. NK cells show spontaneous cytotoxic reactivity against isolated chondrocytes and participate in the rejection of transplanted isolated chondrocytes. Chondrocytes express molecules that can serve as potential antigens in inflammatory joint diseases. Chondrocytes express cartilage-specific membrane antigen (CH65), human cartilage glycoprotein-39 (HC gp-39), hyaluronan binding adhesion molecule CD44, thymocyte antigen-1 (Thy-1) – CD90, signal transducer – CD24, lymphocyte function-associated antigen-3 (LFA-3) – CD58, and type I transmembrane protein Tmp21. On the other hand, although chondrocytes express major histocompatibility complex (MHC) class I and class II molecules, they can also exert immunosuppressive and immunomodulatory effects on immunocompetent cells. Isolated chondrocytes do not trigger an efficient allogeneic immune response in vitro and suppress, in a contact-dependent manner, proliferation of activated T cells. This suppression is associated with the expression by chondrocytes of multiple negative regulators of immune response. Chondrocytes express programmed death-ligand (PD-L), chondromodulin-I and indoleamine 2,3-dioxygenase (IDO), molecules that promote self-tolerance and suppress the immune system.

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Section: Chondrocyte Antigens As Potential Targets In Inflammatory Jomentioning

confidence: 99%

Antigenic and immunogenic properties of chondrocytes. Implications for chondrocyte therapeutic transplantation and pathogenesis of inflammatory and degenerative joint diseases

Osiecka-Iwan¹,

Hyc²,

Radomska-Leśniewska³

et al. 2018

cejoi

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“…A recent study has shown an association between the high expression of CD2/CD58 molecules and RA . CD58 expression is known to be upregulated in inflammatory lesions; this leads to targeted recruitment of T cells into inflammatory sites . CD58 is widely distributed among cell types of the synovial microenvironment and provides numerous cell types with which lymphocytes can interact via CD2 molecule.…”

mentioning

confidence: 99%

Immunosuppression by Co‐stimulatory Molecules: Inhibition of CD2‐CD48/CD58 Interaction by Peptides from CD2 to Suppress Progression of Collagen‐induced Arthritis in Mice

et al. 2013

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Targeting co-stimulatory molecules to modulate the immune response has been shown to have useful therapeutic effects for autoimmune diseases. Among the co-stimulatory molecules, CD2 and CD58 are very important in the early stages of generation of an immune response. Our goal was to utilize CD2-derived peptides to modulate protein-protein interactions between CD2 and CD58, thereby modulating the immune response. Several peptides were designed based on the structure of the CD58 binding domain of CD2 protein. Among the CD2-derived peptides, peptide 6 from the F and C β-strand region of CD2 protein exhibited inhibition of cell-cell adhesion in the nanomolar concentration range. Peptide 6 was evaluated for its ability to bind to CD58 in Caco-2 cells and to CD48 in T cells from rodents. A molecular model was proposed for binding a peptide to CD58 and CD48 using docking studies. Furthermore, in vivo studies were carried out to evaluate the therapeutic ability of the peptide to modulate the immune response in the collagen-induced arthritis (CIA) mouse model. In vivo studies indicated that peptide 6 was able to suppress the progression of CIA. Evaluation of the antigenicity of peptides in CIA and transgenic animal models indicated that this peptide is not immunogenic.

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“…Hoffmann et al, have reported that serum and synovial fluid sCD58 levels in patients with RA were found reduced compared to the levels in normal controls and patients with osteoarthritis (OA) or spondylarthropathy (SpA) [49]. Since soluble CD58 (sCD58) may normally mediate de-adhesion, decreased albumin concentrations due to systemic inflammation may lead to reduced sCD58 levels, thus resulting in increased T cell adhesiveness.…”

Section: Cd2 and Cd58 Roles In Disease Pathologymentioning

confidence: 99%

“…Insufficient release of sCD58, e.g. in synovitis, might result in T cell accumulation and perpetuation of inflammation [49]. In addition, endothelial cells in RA have been shown to express elevated levels of CD58 and in SF, RA lymphocyte expresses increased levels of CD2 and CD58 [50] relative to RA or normal PB lymphocytes.…”

Section: Cd2 and Cd58 Roles In Disease Pathologymentioning

confidence: 99%

Targeting T-Cell Adhesion Molecules for Drug Design

Jois¹,

Liu²,

Nagarajarao³

2006

CPD

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Adhesion molecules participate in many stages of immune response; they regulate leukocyte circulation, lymphoid cell homing to tissues and inflammatory sites, migration across endothelial cells and T-cell stimulation. During T-cell immune response, adhesion molecules form a specialized junction between T-cell and the antigen presenting cell. Thus, many researchers have focused their attention on targeting adhesion molecules for developing therapeutic agents. Most of these efforts are intended to develop drugs for autoimmune and inflammatory diseases. Therapeutic agents like efalizumab and alefacept have been approved by the FDA for the treatment of inflammatory autoimmune diseases. This review focuses on some of the basic aspects and importance of adhesion molecules, recent understanding of the structure of adhesion molecules, and the targeted therapeutic agents.

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Characterization of a soluble form of CD58 in synovial fluid of patients with rheumatoid arthritis (RA)

Cited by 15 publications

References 27 publications

Antigenic and immunogenic properties of chondrocytes. Implications for chondrocyte therapeutic transplantation and pathogenesis of inflammatory and degenerative joint diseases

Antigenic and immunogenic properties of chondrocytes. Implications for chondrocyte therapeutic transplantation and pathogenesis of inflammatory and degenerative joint diseases

Immunosuppression by Co‐stimulatory Molecules: Inhibition of CD2‐CD48/CD58 Interaction by Peptides from CD2 to Suppress Progression of Collagen‐induced Arthritis in Mice

Targeting T-Cell Adhesion Molecules for Drug Design

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