Chemokines play a central role in the pathogenesis of rheumatoid arthritis (RA) synovitis which is characterised by new blood vessel formation, thickening of the lining layer and infiltration of immune cells. The inflammatory infiltrate is generated by a series of events which include the recruitment of leukocytes from the blood stream into the tissue, their local retention and activation to effector cells. All these processes are finely regulated by the interplay of different cell adhesion molecules (CAMs) and chemoattractant factors called chemokines (CK). CK are a superfamily of small proteins that play a crucial role in immune and inflammatory reactions. These chemoattractant cytokines share structural similarities including four conserved cysteine residues which form disulphide bonds in the tertiary structure of the proteins. CK mediate their effects by binding specific receptors (CK-R) characterised by a domain structure which spans the cell membrane seven times and signal through heterotrimeric GPT-binding proteins. Activation of the CK network results in an amplification of the inflammatory cascade and consequently in the progressive destruction of RA joints. The recognition of the central role of CK in inflammation has paved the way to the development of new agents capable of interfering with CK and CK-R. This review will focus in particular on the role of CK in regulating leukocyte trafficking in RA joints.

Ruolo delle chemochine nella patogenesi della sinovite cronica in corso di artrite reumatoide [Role of chemokines in the pathogenesis of chronic synovitis during rheumatoid arthritis] / F. Ingegnoli, A. Manzo, F. Fantini, R. Caporali, C. Montecucco, N. Pipitone, C. Pitzalis. - In: REUMATISMO. - ISSN 0048-7449. - 54:1(2002), pp. 12-18. [10.4081/reumatismo.2002.12]

Ruolo delle chemochine nella patogenesi della sinovite cronica in corso di artrite reumatoide [Role of chemokines in the pathogenesis of chronic synovitis during rheumatoid arthritis]

F. Ingegnoli
Primo
;
F. Fantini;R. Caporali;
2002

Abstract

Chemokines play a central role in the pathogenesis of rheumatoid arthritis (RA) synovitis which is characterised by new blood vessel formation, thickening of the lining layer and infiltration of immune cells. The inflammatory infiltrate is generated by a series of events which include the recruitment of leukocytes from the blood stream into the tissue, their local retention and activation to effector cells. All these processes are finely regulated by the interplay of different cell adhesion molecules (CAMs) and chemoattractant factors called chemokines (CK). CK are a superfamily of small proteins that play a crucial role in immune and inflammatory reactions. These chemoattractant cytokines share structural similarities including four conserved cysteine residues which form disulphide bonds in the tertiary structure of the proteins. CK mediate their effects by binding specific receptors (CK-R) characterised by a domain structure which spans the cell membrane seven times and signal through heterotrimeric GPT-binding proteins. Activation of the CK network results in an amplification of the inflammatory cascade and consequently in the progressive destruction of RA joints. The recognition of the central role of CK in inflammation has paved the way to the development of new agents capable of interfering with CK and CK-R. This review will focus in particular on the role of CK in regulating leukocyte trafficking in RA joints.
Arthritis, Rheumatoid; Autoimmune Diseases; Chemokines; Chemotaxis, Leukocyte; Drug Design; Humans; Models, Biological; Receptors, Chemokine; Synovitis
Settore MED/16 - Reumatologia
Article (author)
File in questo prodotto:
File Dimensione Formato  
mikimos,+La+Rassegna+12-18 (1).pdf

accesso aperto

Tipologia: Publisher's version/PDF
Dimensione 64 kB
Formato Adobe PDF
64 kB Adobe PDF Visualizza/Apri
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/944056
Citazioni
  • ???jsp.display-item.citation.pmc??? 0
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact