Functional genomics of stromal cells in chronic inflammatory diseases

Slowikowski, Kamil; Wei, Kevin; Brenner, Michael B.; Raychaudhuri, Soumya

doi:10.1097/bor.0000000000000455

Cited by 10 publications

(4 citation statements)

References 46 publications

(58 reference statements)

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“…These results suggested that Thy-1 might be a potential biomarker for cartilage pathogenesis, degradation, and metabolic turnover [ 97 , 98 ]. Fibroblasts positive for CD90 were enriched in the synovium of RA patients [ 99 ], but only a minority of RA articular chondrocytes displayed a moderate CD90 expression [ 98 ].…”

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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“…Exposure to inflammation induced by chronic injury, infections, toxins, tissue damage is known to predispose to cancer. OX-S serves to amplify inflammation by activating macrophages and other cells to produce inflammatory peptides [152][153][154][155][156][157][158][159], which disrupt the balance between apoptosis and proliferation in endothelial, vascular smooth muscle, fat, or parenchymal cells. Increased proliferation of adipocytes predisposes to obesity.…”

Section: Agementioning

confidence: 99%

The Framingham Study on Cardiovascular Disease Risk and Stress-Defenses: A Historical Review

Abohelwa

Kopel

Shurmur

et al. 2023

JVD

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The Framingham Heart Study (FHS) began in 1949 with the goal of defining the epidemiology of hypertensive or arteriosclerotic heart disease in the population of Framingham, Massachusetts, a primarily Caucasian suburb west of Boston with a population of approximately 28,000. The participants were without previous symptoms of heart disease and were followed for the occurrence of Cardiovascular Disease (CVD). The study documented a comprehensive medical history that included current symptoms, family history, past cardiac history, social history, and medications. The medical exam included diagnostic studies of chest X-ray, electrocardiogram (EKG), complete blood count (CBC), uric acid level, blood glucose, urinalysis, and venereal disease research laboratory test; Syphilis (VDRL). Serum lipids, recognized at the time to be associated with cardiovascular disease, were also measured. These included cholesterol, total phospholipids, and the Gofman’s Sf 10–20 fraction. Study participants underwent four examinations at 6-month intervals to document any clinical manifestation of CVD. The present understanding of the epidemiologic factors that influence cardiovascular disease risk (CVD-R) is based on the first report of study results at a 6-year median follow-up and numerous subsequent analyses of long-term follow-up data from the original Framingham cohort as well as their offspring. In this paper, we review the Framingham cohort study with regards to the risk factors of peripheral vascular disease.

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“…During clinically apparent RA, innate and adaptive immune cells invade the synovium and together with jointendogenous cells form tissue-destructive lesions. T cells are key pathogenic drivers required for autoantibody production and sustain synoviocyte proliferation, neoangiogenesis, and cartilage and bone erosions (Slowikowski et al, 2018;Weyand and Goronzy, 2006). Multiple genetic polymorphisms associated with RA risk are implicated in T cell receptor signaling (Fonseka et al, 2017;Terao et al, 2016).…”

Section: Introductionmentioning

confidence: 99%