Correlation of activated monocytes or B cells with T lymphocyte subsets in patients with Graves' disease.

González, Álvaro; Calleja, Amparo; Santiago, Esteban; Miguel, Carlos de; López-Zabalza, Marı́a J.; López-Moratalla, N

doi:10.3892/ijmm.1.1.95

Cited by 5 publications

(4 citation statements)

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“…The increase in the proportion of CD14 CD16 DR monocytes, as well as the decrease in the proportion of CD14 monocytes are in agreement with observations reported by others [33^35], who consider the CD14 cells as small mature blood monocytes, and seemingly having their origin in the maturation of CD14 monocytes. An evolution of monocytes towards macrophages, similar to that induced by peptide Pa, has also been described as being operative in patients with multiple sclerosis [13], or Graves' disease [36]. Furthermore, a correlation of iNOS, CD16 and HLA-DR has already been described by us [13].…”

Section: Discussionmentioning

confidence: 81%

Co-expression of inducible nitric oxide synthase and arginases in different human monocyte subsets. Apoptosis regulated by endogenous NO

Rouzaut¹,

Subirá²,

Miguel³

et al. 1999

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Human monocyte subsets, isolated from cultures of mononuclear cells, or freshly obtained from patients with multiple sclerosis, Graves' disease or pemphigus vulgaris, differed in phenotype, apoptotic features, mRNA levels of arginase II (A-II) and the inducible form of nitric oxide synthase (iNOS). Liver-type arginase I mRNA was present in all subsets. Apoptosis was followed by the expression of T cell intracellular antigen (TIA) and the simultaneous detection of DNA stainability by propidium iodine and annexin V binding. Apoptosis was practically absent both in activated CD14(++)CD33(++)DR(++)CD25(++)CD69(++)CD71(++/+) CD16(-) cells, expressing A-II mRNA and having arginase activity, but not iNOS mRNA, and in not fully mature large CD14(++)CD16(+)CD23(+)DR(++) monocytes, expressing simultaneously both mRNAs and having both enzyme activities. However, differentiated small CD14(+/++)CD16(+)CD69(+)CD25(+/-)CD71(++)CD23(+) DR(++) monocytes, expressing high levels of iNOS mRNA, exhibited apoptotic signs. Amounts of NO synthesised by monocytes co-expressing iNOS and arginase changed with the addition of arginine or an iNOS inhibitor; in that case a correlation of NO production and apoptotic features was observed. Data suggest a regulatory role for endogenous NO in apoptosis of stimulated and differentiated monocytes, and also that iNOS and A-II, when simultaneously present, could control the production of NO as a consequence of their competition for arginine.

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Section: Discussionmentioning

confidence: 81%

Co-expression of inducible nitric oxide synthase and arginases in different human monocyte subsets. Apoptosis regulated by endogenous NO

Rouzaut¹,

Subirá²,

Miguel³

et al. 1999

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…In contrast to the predominant CD14 hi /CD16 − phenotype, this subset normally comprises 8% of all circulating monocytes, subdivides into immature large CD14 hi /CD16 + and differentiated small CD14 +/hi /CD16 + cells, exhibits features of tissue M φ and greatly expands in inflammatory disease [34, 35]. In fact, all stages of GD are associated with a generally advanced stage of monocytic differentiation as well as a greater abundance of CD14 + /CD16 + cells [36]. In TAO, excess TNF‐ α may thus lead to the obvious loss in blood monocytes by consumptively differentiating CD14 + /CD16 + cells into intraorbital inflammatory macrophages.…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of TNF/TNFR Superfamily Members: A Systemic Link Between Intra‐ and Extrathyroidal Manifestations in Graves’ Disease

Quadbeck

Stucke²,

Eckstein

et al. 2006

Scand J Immunol

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Graves’ disease (GD) coincides with the occurrence of disease‐associated intrathyroidal dendritic cells (DC) and intraorbital inflammatory macrophages (Mφ). Physiologically, tumour necrosis factor‐α (TNF‐α) strongly affects the differentiation of DC and Mφ from monocytic precursors; we thus hypothesized that dysregulation of the TNF/TNFR superfamilies may provide a systemic pathogenic link in GD. In patients without eye symptoms, percentages of TNF‐α‐stimulated blood monocytes were highly significantly (P < 0.001) elevated, corresponding to both intrathyroidal DC maturation as well as increases in mature blood DC (MHC‐IIhi/CD40+/RFD1hi) and B cells (CD20hi/CD40+). GD patients also displaying eye symptoms revealed a striking reduction in blood monocytes, yet significantly (P < 0.05) increased CD40hi and TNF‐αhi leucocytes. These findings suggest for GD that excess TNF‐α induces monocytes to differentiate into hyperactivated thyroidal DC that, once emigrated, initiate systemic humoral autoimmunity associated with CD40/TNF‐α upregulation. Such overexpression may instigate differentiation of periorbital inflammatory Mφ from CD14hi/CD16+ monocytes as a likely precursor subset. These results indicate that dysregulation of TNF/TNFR superfamily members provides a systemic pathogenic link in GD in that hyperactivated circulating monocytic precursors give rise to locally restricted, disease‐associated DC and Mφ. Monocytes, therefore, may serve as a suitable target to therapeutically address the common precursor of key promoters of GD.

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“…However, very few studies have focused on the subsets of monocytes in GD. The first report analyzing the phenotypic characteristics of monocytes was published in 1998 and found that CD14+ CD16+ DR high monocytes were abundant and correlated with CD4 + CD45 + RO + memory lymphocytes in GD patients 15 . The increased CD14+ CD16+ DR high monocytes were thought to be involved in the repeated presentation of autoantigens or mimetic antigens to helpers T cells in GD.…”

Section: Introductionmentioning

confidence: 99%

Expansion of inflammatory monocytes in periphery and infiltrated into thyroid tissue in Graves’ disease

Chen

Wang

et al. 2021

Sci Rep

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Monocytes are important mediators of immune system and are reported to be altered in autoimmune disorders. Little is known about the pathological role of monocytes in Graves’ disease (GD). Thus, we investigated monocytes in periphery and thyroid tissue in GD. Untreated GD patients were enrolled and followed up until remission. Monocytes were significantly increased and positively correlated with anti-thyrotropin receptor antibody (TRAb) in untreated GD (rcounts = 0.269, P < 0.001; rpercentage = 0.338, P < 0.001). Flow cytometry showed CD14++ CD16+ monocytes were increased and CD14++ CD16- monocytes were decreased in untreated GD (both P < 0.001). Skewed monocyte subsets were recovered in GD with remission. Serum B cell-activating factor (BAFF) was positively correlated with TRAb (r = 0.384 and P = 0.001). CD14++ CD16+ monocytes expressed higher level of BAFF in untreated GD (P < 0.05). The frequency of CD14+ monocytes and CD14+ CD16+ monocytes were significantly higher in GD thyroid tissue than in normal thyroid tissue (both P < 0.001). Our study suggested CD14++ CD16+ monocytes were significantly expanded and involved in the production of TRAb via secreting a higher level of BAFF in periphery. Besides, monocytes infiltrated into thyroid tissue and thus could serve as an important participant in GD pathogenesis.

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Correlation of activated monocytes or B cells with T lymphocyte subsets in patients with Graves' disease.

Cited by 5 publications

References 0 publications

Co-expression of inducible nitric oxide synthase and arginases in different human monocyte subsets. Apoptosis regulated by endogenous NO

Co-expression of inducible nitric oxide synthase and arginases in different human monocyte subsets. Apoptosis regulated by endogenous NO

Dysregulation of TNF/TNFR Superfamily Members: A Systemic Link Between Intra‐ and Extrathyroidal Manifestations in Graves’ Disease

Expansion of inflammatory monocytes in periphery and infiltrated into thyroid tissue in Graves’ disease

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