Expression of CD69 antigen on synovial fluid T cells in patients with rheumatoid arthritis and other chronic synovitis.

Afeltra, Antonella; Galeazzi, Mauro; Ferri, Gm; Amoroso, Antonio; Pità, Ornella De; Porzio, F; Bonomo, Lorenzo

doi:10.1136/ard.52.6.457

Cited by 54 publications

(40 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The CD69 to CD3 ratio of PBMCs was correlated with SLE disease activity index score in SLE [26]. The percentage of T lymphocytes bearing CD69 was significantly increased in synovial fluid from patients with RA [27]. Although Athreya et al [8] have shown that physiological concentrations of PRL did not have any consistent effects on the T lymphocyte subsets in vitro, in our experiment the enhancement of CD69 expression by PRL was significantly recognized on CD8+ cells.…”

Section: Discussioncontrasting

confidence: 32%

Enhanced Expression of CD69 and CD25 Antigen on Human Peripheral Blood Mononuclear Cells by Prolactin

et al. 2005

View full text Add to dashboard Cite

Abstract. Several clinical reports have suggested that prolactin (PRL) plays an important role in the pathogenesis of autoimmune diseases such as rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE). We have investigated the influence of PRL on immune system, by evaluating the effects of PRL on the expression of CD69 and CD25 on human peripheral blood mononuclear cells (PBMCs). Human PBMCs obtained from healthy female volunteers were incubated with phytohemagglutinin (PHA) in the presence or absence of various concentrations of PRL. The expression of CD69 and CD25 was monitored using immunofluorescence staining and flow cytometry. PRL significantly enhanced the expression of CD69 and CD25 on activated PBMCs compared with that in the absence of PRL (p<0.05, paired t-test). Increasing doses of PRL enhanced the expression of CD69 up to 2 mg/ml and CD25 up to 1 mg/ml. The enhanced expression of CD69 was observed on CD8+ T lymphocytes but not on CD4+ T lymphocytes. Our data suggest that PRL can significantly enhance the expression of CD69 and CD25 molecule on human PBMCs when induced by PHA. However, PRL would have to be at optimal concentration in order to enhance their expression. PROLACTIN (PRL) is a pituitary hormone which is known to induce the synthesis of milk proteins in women during breastfeeding [1]. Of particular interest, however, is the role of PRL in immune regulation. Evidence suggests that the immune system is an important target of pituitary PRL, and that PRL may play a physiological role in the regulation of cell-mediated and humoral immune response [2]. It has been shown that PRL has an important role in regulating T lymphocyte-mediated immune functions [3,4]. Receptors for PRL on human lymphocytes have been identified on T and B lymphocytes [5][6][7].On the other hand, T lymphocytes express de novo several cell surface glycoproteins, which are also called activation inducer molecules, in a characteristic order during activation. CD69, one of the earliest of the cell surface activation markers, is a phosphorylated 28-32-kilodalton disulphide linked homodimer. Once expressed, CD69 is thought to take part in the ongoing activation process. CD25 (the a chain of the IL-2 receptor), a phosphorylated 55-60-kilodalton cell surface glycoprotein, is also an activation marker induced during lymphoid cell activation. The synthesis of CD25, along with the IL-2 itself, is induced by the activation of T lymphocytes on the initial encounter with specific antigen. In this report, we have examined the effects of PRL on the expression of CD69 and CD25 antigen on human peripheral blood mononuclear cells (PBMCs). We have found that exogenously-added PRL could significantly enhance the expression of CD69 and CD25 antigen on human PBMCs.

show abstract

Section: Discussioncontrasting

confidence: 32%

Enhanced Expression of CD69 and CD25 Antigen on Human Peripheral Blood Mononuclear Cells by Prolactin

et al. 2005

View full text Add to dashboard Cite

show abstract

“…Venables [16] reported decreased counts of B cells and increased CD8+ cells in SF. In the study of Afeltra et al [ 18] the percentage of T cells bearing CD69 (an early activation marker) was significantly increased in SF of patients with rheumatoid arthritis. In our study, the majority of the lymphocytes in SF were CD3+ T cells (73.1%).…”

Section: Discussionmentioning

confidence: 97%

Study of pro-inflammatory (TNF-?, IL-1?, IL-6) and T-cell-derived (IL-2, IL-4) cytokines in plasma and synovial fluid of patients with juvenile chronic arthritis: Correlations with clinical and laboratory parameters

1998

View full text Add to dashboard Cite

Acute phase proteins, synovial fluid (SF) cellular infiltrates, pro-inflammatory (TNF-alpha, IL-1alpha, IL-6) and Th1 (IL-2) and Th2 (IL-4) derived cytokine levels both in plasma and SF were examined in pauciarticular and polyarticular juvenile chronic arthritis (JCA) patients during the active (n = 22) and inactive (n = 14) period in order to determine pathogenic mechanisms and correlations between cytokines and laboratory parameters showing disease activity. The erythrocyte sedimentation rate (ESR), serum C-reactive protein (CRP) and IgG concentrations were found to be significantly elevated in the active period of JCA. In pauciarticular JCA patients, when compared with their peripheral blood lymphocyte subpopulations, SF CD3+ cells (73.1%) and HLA-DR+ active T cells (22.5%) were found to be significantly increased. In the active period of JCA, plasma TNF-alpha and IL-6 concentrations were significantly elevated. Plasma IL-2 and IL-4 levels were not elevated and were found to be similar to those in the inactive phase and in healthy controls. SF IL-6, TNF-alpha and IL-1alpha levels were extremely high in all the patients. SF IL-4 and IL-2 levels were all undetectable. There was a significant correlation between ESR values and plasma IL-6 levels and between serum CRP levels and plasma IL-6 and TNF-alpha concentrations. In conclusion, increased local production of pro-inflammatory cytokines appears to account for the articular manifestations of JCA. The impaired production of anti-inflammatory Th2-derived cytokines (IL-4) seems to cause increased production of inflammatory cytokines acting on the balance between them. The deficit in IL-2 production was not suggested to be primarily involved in the pathogenesis. In addition, not only CRP and ESR values, but also plasma IL-6 and TNF-alpha concentrations may be used as markers of disease activity.

show abstract

“…It is required for antigen presentation and activation of helper Tlymphocytes. 14,19,23) They respectively expressed in some inflammatory infiltrates and played important roles in the pathogenesis of some inflammatory diseases such as allergic airway inflammation, 18,24) rheumatoid arthritis, 15) psoriasis vulgaris lesional skin, 16) and active inflammatory bowel disease, 17) . Thus, the increases in CD69 and HLA-DR on CD3 + T-lymphocytes implied there is an activation of peripheral blood CD3 + T-lymphocytes in AF patients.…”

Section: Discussionmentioning

confidence: 99%

“…14) They both play a role in the specific immune response to inflammation. [13][14][15][16][17][18][19][20] To our knowledge, there is little information available about the expression of CD69 and HLA-DR on peripheral blood CD3 + T-lymphocytes in patients with AF. In this study, we investigated the relationship between the activation of peripheral blood CD3 + T-lymphocytes and AF by flow cytometric analysis with the aim of providing more evidence to support this phenomenon.…”

mentioning

confidence: 99%

Activation of Peripheral Blood CD3<sup>+</sup> T-lymphocytes in Patients With Atrial Fibrillation

Liu

Lee

et al. 2012

Int. Heart J.

View full text Add to dashboard Cite

SummaryAtrial fibrillation (AF) is a common disease with a poorly understood pathophysiological mechanism. Increasing evidence indicates that AF may be associated with immunologic inflammation responses, but it remains unclear whether activation of peripheral blood CD3 + T-lymphocytes plays a role in the pathogenesis of AF. The aim of this study was to evaluate this phenomenon. Fifty paroxysmal AF patients and 56 persistent AF patients who underwent successful electrical cardioversion were enrolled. The percentages of CD69 and human leukocyte antigen DR (HLA-DR) positive peripheral blood CD3 + T-lymphocytes, which indicate T-lymphocyte activation, were examined by flow cytometric analysis in the patients and 51 healthy controls. The patient groups had higher levels of CD69 and HLA-DR than the healthy controls. During the 3-month follow-up, 37 patients had recurrence of AF (recurrence group) and 50 patients remained in sinus (sinus group). The CD69 and HLA-DR levels in the sinus group were all significantly down-regulated at follow-up compared with before cardioversion. However, there were no statistically significant differences between the CD69 and HLA-DR levels in the recurrence group at follow-up and before cardioversion. Our findings suggest that activation of peripheral blood CD3 + T-lymphocytes was associated with AF, and might be a diagnostic or therapeutic marker. (Int Heart J 2012; 53: 221-224)

show abstract

Expression of CD69 antigen on synovial fluid T cells in patients with rheumatoid arthritis and other chronic synovitis.

Cited by 54 publications

References 13 publications

Enhanced Expression of CD69 and CD25 Antigen on Human Peripheral Blood Mononuclear Cells by Prolactin

Enhanced Expression of CD69 and CD25 Antigen on Human Peripheral Blood Mononuclear Cells by Prolactin

Study of pro-inflammatory (TNF-?, IL-1?, IL-6) and T-cell-derived (IL-2, IL-4) cytokines in plasma and synovial fluid of patients with juvenile chronic arthritis: Correlations with clinical and laboratory parameters

Activation of Peripheral Blood CD3<sup>+</sup> T-lymphocytes in Patients With Atrial Fibrillation

Contact Info

Product

Resources

About