Rheumatoid Arthritis: Pennec YL

Youinou P, Pers JO, Saraux A, Pennec YL. · No affiliation provided · Clin Exp Immunol. · Pubmed #15958065 links to  free full text

This publication has no abstract.

Roguedas AM, Youinou P, Lemasson G, Pennec YL, Misery L. · Laboratory of Immunology, Brest University Medical School, 2 avenue Foch, 29609 Brest Cedex, France. · J Eur Acad Dermatol Venereol. · Pubmed #16503880 No free full text.

Abstract: Gougerot-Sjögren syndrome (GSS) is a chronic heterogeneous non-organ-specific autoimmune disease, encompassing a wide spectrum of clinical manifestations. It is characterized by a lymphocytic infiltration of the exocrine glands, also called epitheliitis, resulting in xerostomia and keratoconjunctivitis sicca. The skin can also be involved; for example, xerosis is a consequence of epitheliitis. Dermatological consequences of polyclonal reactivity are vasculitis and manifestations of B-cell proliferation vary from plasma cell infiltrates to B-cell lymphoma.

Roguedas AM, Misery L, Sassolas B, Le Masson G, Pennec YL, Youinou P. · Laboratory of Immunology, Brest University Medical School, Brest, France. · Clin Exp Rheumatol. · Pubmed #15485020 No free full text.

Abstract: The association of kerato-conjunctivitis sicca and xerostomia has been termed Sjogren's syndrome (SS). Although this disease is referred to as a non-organ-specific autoimmune condition, the vast majority of the deleterious effects of primary SS are restricted to the exocrine glands. Among them, the lacrymal and salivary glands are at the foreground, owing to the severity of the objective consequences and the importance of the subjective manifestations. As a result, cutaneous manifestations are minimized, albeit relatively common. We have carefully analyzed the literature to draw up an inventory of the possible skin complications of this syndrome. In addition to xerosis and epidermal IgG deposits, they include vasculitis and cutaneous B cell lymphoma. Alopecia, vitiligo and papular lesions have also been reported to be associated with primary SS.

Mamoune A, Durand V, Le Goff P, Pennec YL, Youinou P, Le Corre R. · Laboratory of Immunology, Brest University Medical School, France. · Histol Histopathol. · Pubmed #10809380 No free full text.

Abstract: CD45RO+ T cells are referred to as memory or helper-inducer while CD45RA+ T cells are regarded as naive or suppressor-inducer T cells. The former population predominates in the peripheral blood and even more in the synovial fluid of patients with rheumatoid arthritis, to the expense of the latter population. Within the CD45RB+ compartment, there appears to be more of the fully-differentiated than of the early-differentiated CD4+ T cells. In spite of the fact that these lymphocytes are close to undergoing apoptosis, this programmed cell death is inhibited in the rheumatoid synovium.

Daridon C, Pers JO, Devauchelle V, Martins-Carvalho C, Hutin P, Pennec YL, Saraux A, Youinou P. · Laboratory of Immunology, Brest University Medical School Hospital, BP824, F-29609 Brest, France. · Arthritis Rheum. · Pubmed #16802367 links to  free full text

Abstract: OBJECTIVE: To identify B cell subpopulations participating in the lymphocyte infiltrate of salivary glands from patients with primary Sjögren's syndrome. A special emphasis was placed on those B lymphocytes included in the ectopic germinal centers (GCs). METHODS: The presence of B cells in salivary glands and their polyclonality were ascertained by phenotyping and reverse transcription-polymerase chain reaction in salivary gland samples from 18 patients. Their phenotype was thoroughly analyzed using a number of double-staining combinations. The results obtained in tissue sections were confirmed by fluorescence-activated cell sorting analysis of B cells eluted from salivary glands, and these findings were compared with those in tonsils. RESULTS: Memory-type B cells were defined as CD20+, CD27+ and were seen in all specimens, whereas GCs were found in only 7 specimens. Furthermore, B cells found in these GCs lacked certain characteristics of centroblasts and centrocytes. Instead, they fulfilled the criteria for transitional type II (TII) B cells and resembled marginal-zone B cells. BAFF (the assistance of which is required for proper transformation of transitional TI B cells into transitional TII B cells) accumulated adjacent to transitional and marginal-zone-like B lymphocytes. Further evidence for the involvement of BAFF came from the expression of its receptors on infiltrating B cells. CONCLUSION: These transitional TII and marginal-zone-like B cells are probably instrumental in the local production of autoantibodies and possibly influential in the ensuing destruction of epithelial cells.

Pers JO, d'Arbonneau F, Devauchelle-Pensec V, Saraux A, Pennec YL, Youinou P. · Brest University Medical School, France. · Arthritis Rheum. · Pubmed #16052575 links to  free full text

Abstract: OBJECTIVE: To correlate the periodontal status of 15 patients with primary Sjögren's syndrome (SS) with their salivary levels of BAFF. METHODS: The periodontal status of 15 patients who fulfilled the criteria for primary SS was compared with that of 15 controls with xerostomia who did not fulfill the criteria for primary SS but had similar symptoms of dry mouth. The level of BAFF was measured in paired samples of saliva and serum using in-house enzyme-linked immunosorbent assays. Periodontitis was assessed by the plaque index, the modified gingival index, the papillary bleeding index, and the periodontal pocket depth. RESULTS: Notwithstanding the better oral hygiene practices of the patients with primary SS compared with those of the xerostomia controls and the subsequent reduction of their plaque index scores, complications of periodontitis, such as bleeding, gingival hypertrophy, and periodontal pockets, were not improved. This failure to ameliorate the complications of periodontitis in patients with primary SS was associated with high levels of BAFF in their saliva compared with the levels in xerostomia controls (7.4 +/- 2.1 versus 1.0 +/- 0.4 ng/ml [P < 0.002]). The levels of BAFF in saliva did not correlate with the levels in sera but did correlate with the periodontal pocket depth (P < 0.002). CONCLUSION: These findings are similar to the bone resorption observed in patients with rheumatoid arthritis. They suggest that the known effect of B cells in periodontitis would be partly mediated by salivary BAFF in patients with primary SS.

D'Arbonneau F, Ansart S, Le Berre R, Dueymes M, Youinou P, Pennec YL. · Laboratory of Immunology, Brest University Medical School Hospital, F-29609 Brest Cedex, France. · Arthritis Rheum. · Pubmed #14673967 links to  free full text

Abstract: OBJECTIVE: To evaluate the prevalence of thyroid dysfunction and related autoantibodies in patients with primary Sjögren's syndrome (pSS), and to determine whether these abnormalities develop over time. METHODS: pSS patients (n = 137) and controls (n = 120) were investigated for thyroid dysfunction and for the presence of anti-thyroid peroxidase antibody (anti-TPO) and antithyroglobulin antibody (ATG). Followup time for patients was 1-16 years, and 72 of the 120 controls were reevaluated 3 years after initial evaluation. RESULTS: Thyroid disease was more frequent in the pSS patients than in the controls (30% versus 4%; P < 10(-4)), as were anti-TPO and ATG (11% versus 3%; P < 0.02, and 3% versus 1%, not significant). Ten of 107 euthyroid pSS patients dropped out of the study, and thyroid dysfunction became apparent at followup in 12 of the remaining 97. Most of the patients with thyroid-related autoantibodies at entry developed autoimmune thyroid disease thereafter. CONCLUSION: Thyroid dysfunction is frequent in pSS patients, and those prone to develop thyroid disorders are identified by thyroid-related autoantibodies, or by rheumatoid factor and anti-Ro/SSA activity.

Basset C, Durand V, Mimassi N, Pennec YL, Youinou P, Dueymes M. · Laboratory of Immunology; Department of Internal Medicine, Institut de Synergie des Sciences et de la Santé (I3S), Brest University Medical School, Brest, France. · Scand J Immunol. · Pubmed #10736101 No free full text.

Abstract: Despite the indisputable role of immunoglobulin (Ig)A in the pathogenesis of primary Sjögren syndrome (pSS), the causative abnormality remains largely unknown. As an extension of our report that IgA is oversialylated in this disease, the thrust of the present study was to measure the sialyltransferase (ST) activity in B lymphocytes. ST containing lysates of B cells from 17 pSS patients and 10 controls, were obtained using a combination of detergents, and incubated with affinity purified IgA that had been previously desialylated. The deposition of cytidine 5' monophosphate sialic acid (SA) by ST from B cells onto IgA was detected by two ELISA based upon the use of biotinylated lectins (Sambucus nigra agglutinin which is specific for alpha2-6 SA and Maackia amurensis which is specific for alpha2-3 SA). In parallel, the amount of SA on IgA from ten of the 17 patients and eight of the 10 controls was assayed using the same method. An excess of alpha2-3 and alpha2-6 SA on IgA was found in those patients with excessive activity of alpha2-3 and alpha2-6 ST. Thus, IgA hypersialylation in pSS patients may result from undue activity of ST.

Basset C, Devauchelle V, Durand V, Jamin C, Pennec YL, Youinou P, Dueymes M. · Brest University Medical School, Brest, France. · Scand J Immunol. · Pubmed #10607305 No free full text.

Abstract: Immunoglobulin A (IgA), which is heavily glycosylated, interacts with a variety of receptors, e.g. the asialoglycoprotein receptor (ASGP-R), which binds terminal galactose residues, and the Fcalpha receptor (FcalphaRI). It has thus been proposed that elevated serum levels of IgA in primary Sjögren's syndrome (pSS) are caused by its defective clearance. To test this hypothesis, we developed a method (based on sialyl transferases eluted from a hepatoma cell line) to increase the amount of sialic acid (SA) on IgA, and used a battery of IgA1- and IgA2-specific glycosidases to reduce this amount. Binding of IgA1 and IgA2 to ASGP-R and FcalphaRI was found to be sugar dependent because oversialylated IgA bound less than native or desialylated IgA. However, individual sugars did not play a direct role in this binding. Given that IgA are oversialylated in pSS, defective clearance of IgA may indeed be ascribed to an excess of SA in IgA1 and IgA2.