湿疹及皮炎

20053708异位性皮炎患者外用血Th2细胞分化偏态性分析/吴江(广州市一院),曾仁山∥中国麻风皮肤病杂志.2005,21(80).616～617采用三色流式细胞术测定20例异位性皮炎患者和30例健康对照者外周血趋化性细胞因子受体CCR4+CD4+T和CXCR3+CD4+细胞的表达水平。结果显示患者外周血CCR4+CD4+细胞水平明显高于对照组(P<0.01);CCR4/CXCR3比率明显高于对照组(P<0.01);CXCR3+CD4+T细胞的水平与对照组差异无统计学意义(P>0.05)。提示异位性皮炎患者外周血T细胞亚群分化失衡,Th2细胞和异位性皮炎发生、发展有关。表1参11(张美芳)20053709特…     

异位性皮炎患者外周血Th2细胞分化偏态性分析

为了探讨异位性皮炎患者外周血辅助性T（Th）细胞亚群分化表达及其在异位性皮炎发病过程中的作用．采用三色流式细胞术测定20例异位性皮炎患者和30例健康对照者外周血趋化性细胞因子受体CCR4^＋ CD4^＋T和CXCR3^＋ CD4^＋T细胞的表达水平、异值性皮炎患者外周血CCR4^＋ CD4^＋T细胞水平明显高于对照组（P〈0.01）；异位性皮炎患者外周血CCR4／CXCR3比率明显高于对照组（P〈0．01）；异位性皮炎患者外周血CXCR3^＋CD4^＋T细胞的水平与对照组差异无统计学意义（P〉0．05）、异位性皮炎患者外周血T细胞亚群分化失衡．Th2细胞和异化性皮炎发生、发展有关。     

尖锐湿疣患者趋化性细胞因子及其受体的研究

目的研究尖锐湿疣(CA)患者血清趋化性细胞因子及其受体表达的变化在发病机理中的作用。方法采用酶联免疫吸附试验检测30例CA患者及正常人血清中白介素8(IL鄄8)、γ干扰素诱导蛋白10(IP鄄10)、单核细胞趋化蛋白1(MCP鄄1)、巨噬细胞炎性蛋白1α(MIP鄄1α)、活化后可调节的、正常T细胞表达和分泌的因子(RANTES)及巨噬细胞来源的趋化性细胞因子(MDC)等水平变化。同时用流式细胞仪分析20例CA患者外周血CD3+T淋巴细胞表面趋化性细胞因子受体CXCR1、CXCR3、CCR2及CCR5的表达。结果与正常人对照组相比,CA患者血清IP鄄10和MIP鄄1α水平显著升高(P<0.02和P<0.05),外周血CXCR1+T细胞百分率显著增加(P<0.05)。结论CA患者血清IP鄄10和MIP鄄1α水平及外周血CXCR1+T细胞百分率增高,并与疾病的复发和病程的长短有关。IP鄄10和MIP鄄1α在机体非特异性抗病毒免疫应答中起着重要作用。     

中重度特应性皮炎患者外周血IL-31水平及IgE表达与临床相关性

目的检测中重度特应性皮炎患者外周血白细胞介素(IL)-31及IgE的水平、CD4~+T细胞的活化。方法中重度特应性皮炎患者18例及健康对照者25例,抽取外周静脉血,流式细胞仪检测CD3~+CD4~+CD69~+T细胞百分比,ELISA检测血清中IL-31、IgE的水平。结果中重度特应性皮炎患者外周血CD3~+CD4~+CD69~+T细胞百分比明显升高(P0.01)。外周血IL-31及IgE的水平均明显升高(P0.01),与SCORAD评分均有显著性相关(P0.01)。结论特应性皮炎患者体内T细胞被信号分子激活活化,从而可能促进细胞因子的分泌而加重临床症状。     

特应性皮炎患儿外周血T细胞亚群与总IgE水平的相关性研究

目的探讨儿童特应性皮炎的外周血T细胞亚群水平及其与总IgE水平的相关性。方法采用流式细胞分析技术及荧光酶联免疫法对18例特应性皮炎患儿和18例正常儿童外周血T细胞亚群及总IgE水平进行测定。结果特应性皮炎患儿外周血CD4+、CD4+/CD8+比值均高于正常对照组(p0.01,p0.05),CD8+低于正常对照组(p0.05)。IgE增高特应性皮炎组CD4+、CD4+/CD8+比值均高于IgE正常组(p0.01,p0.05)和正常对照组(p0.01,p0.05),CD8+低于正常对照组(p0.05);IgE正常组CD4+、CD8+、CD4+/CD8+比值与正常对照组比较均无显著性差异(p0.05)。结论儿童特应性皮炎存在免疫功能失衡,表现为CD4+T细胞增多,功能亢进,CD8+T细胞不足导致免疫功能紊乱。T细胞亚群变化与总IgE水平增高相关。     

特应性皮炎患者外周血表达不同细胞因子T细胞亚群的检测

目的 探讨特应性皮炎患者外周血表达不同细胞因子T细胞群的频数及其与疾病严重程度的相关性。方法 采用流式细胞仪，检测外周血表达不同胞质内细胞因子（包括IL-4、IL-5、IFN-γ、TNF-α）的CD4+ T、CD8+ T、CLA+ T细胞亚群的频数。利用特应性皮炎皮损面积严重度指数积分法方法，获取特应性皮炎患者病情严重程度积分，分析其与表达不同细胞因子的T细胞频数的相关性。结果 特应性皮炎患者外周血中，胞质内表达IL-4和IL-5的CD4+ T、CD8+ T、CLA+ T细胞频数均高于对照组，胞质内表达IFN-γ的CD4+ T、CLA+ T细胞频数低于对照组；差异均有统计学意义。患者组与正常人对照组中，TNF-α在不同T细胞亚群中表达差异无统计学意义。疾病严重程度与IL-4+CD4+ T细胞和IL-5+CLA+ T细胞群的表达频数相关。结论 患者外周血T细胞存在免疫偏移，表达某些细胞因子的T细胞亚群水平可能作为检测疾病严重程度的指标。     

特应性皮炎患者趋化因子及其受体的研究

目的 探讨几种重要的趋化因子及其受体的表达在特应性皮炎(AD)发病中的作用。方法 采用酶联免疫吸附试验检测39例AD患者及正常人血清中γ干扰素诱导蛋白-10(IP-10)、基质细胞衍生因子-1α(SDF-1α)、嗜酸粒细胞趋化因子、胸腺和活化调节的趋化因子(TARC)及巨噬细胞来源的趋化因子(MDC)等水平;同时用流式细胞仪分析外周血CD4⁺T细胞表面趋化因子受体CXCR3、CXCR4、CCR3、CCR4及CCR5的表达。结果 与正常人对照组相比,AD患者血清SDF-1α、TARC和MDC水平显著升高(P<0.001),IP-10及嗜酸粒细胞趋化因子水平则无明显改变(P>0.05),外周血CXCR3、CCR3、CCR4及CCR5在CD4⁺T细胞表达水平显著增加(P<0.001);血清TARC和MDC水平的变化与疾病严重程度相关(r分别为0.669及0.409,P分别为<0.001及<0.01)。结论 具有生物活性趋化因子及其受体介导的T细胞和嗜酸/嗜碱粒细胞的聚集、激活后释放的炎性介质在AD发病中起着重要作用。     

复发性生殖器疱疹患者外周血T细胞CD69和HLA-DR的表达

目的:探讨复发性生殖器疱疹(RGH)患者外周血CD69和HLA-DR分子在T细胞的表达。方法:采用免疫荧光三标记流式细胞术检测18例RGH患者在疾病发作期和静止期外周血T细胞上CD69和HLA-DR抗原的表达。结果:RGH患者外周血CD3+T细胞CD69的表达,较正常对照组明显升高(P<0.01);CD4+T细胞CD69的表达,在发作期为5.63±1.74,静止期为7.12±2.27,均比正常对照组明显升高,发作期与静止期相比差异有高度显著性(P<0.01);RGH患者外周血CD3+T细胞HLA-DR+的表达,亦显著高于对照组(P<0.01)。结论:单纯疱疹病毒感染诱导体内CD4+和CD8+T细胞活化、增殖,前者分泌多种抗病毒细胞因子,后者则分化为病毒特异性CD8+细胞毒T细胞,它们共同发挥着抗病毒作用。     

特应性皮炎患者外周血皮肤归巢的CD8+ T细胞研究

【摘要】 目的 探讨特应性皮炎（AD）患者外周血CD8+ T细胞皮肤归巢及杀伤功能相关蛋白的表达。 方法 15例AD患者和14例健康人,用流式细胞仪,检测外周血CD8+ T细胞、表达皮肤淋巴细胞相关抗原的CD8+ T细胞（CLA+CD8+ T细胞）的比例。 结果 CD8+ T细胞比例在AD组和对照组之间差异无统计学意义（P > 0.05）;CD8+ T细胞穿孔素、颗粒酶B和FasL的表达在两组间差异亦无统计学意义（均P > 0.05）。CLA+CD8+ T细胞比例在AD组（3.80% ± 1.46%）高于健康对照组（2.18% ± 0.85%）（t = 3.636,P < 0.01）,AD组CLA+CD8+ T细胞比例与SCORAD（SCORing of Atopic Dermatitis）评分呈正相关（r = 0.565,P < 0.05）;CCR4在CD8+ T细胞表达在AD组（13.86% ± 4.42%）高于健康对照组（9.50% ± 2.14%）（t = 3.738,P < 0.01）,而CCR10和CXCR6的表达在两组间差异均无统计学意义（P > 0.05）。CLA+CD8+ T细胞穿孔素的表达在AD组（74.27% ± 15.94%）高于健康对照组（57.20% ± 14.64%）（t = 2.998,P < 0.01）,颗粒酶B的表达在AD组（70.90% ± 13.85%）也高于健康对照组（56.41% ± 11.00%）（t = 3.104,P < 0.01）,而FasL的表达在两组间差异无统计学意义（P > 0.05）。CLA+CD8+ T细胞CCR4、CCR10和CXCR6的表达在AD组与对照组间差异无统计学意义（均P > 0.05）。 结论 AD患者外周血CLA+CD8+ T细胞数量增加,杀伤功能相关蛋白穿孔素、颗粒酶B的表达增强,可能参与了AD的发病。     

系统性红斑狼疮患者糖皮质激素受体与T淋巴细胞亚群的研究

目的探讨系统性红斑狼疮(SLE)患者外周血淋巴细胞糖皮质激素受体及T淋巴细胞亚群的变化。方法用放射性配基结合一点分析法及碱性磷酸酶抗碱性磷酸酶法,测定30例SLE患者外周血淋巴细胞糖皮质激素受体及T淋巴细胞亚群,并与20例正常对照组相比较。结果SLE患者外周血淋巴细胞糖皮质激素受体为3654±459结合位点细胞,与正常对照组(4839±575结合位点细胞)相比,显著降低,差异有显著性(P<0.01);SLE患者外周血CD3+T细胞、CD4+T细胞及CD4+CD8+比值与正常对照组相比,显著降低,差异有显著性(P<0.01);CD8+T细胞亦降低,与正常对照组相比,差异无显著性(P<0.05)。结论SLE患者存在免疫调节功能的紊乱,SLE患者外周血淋巴细胞的糖皮质激素受体水平降低,可能在一定程度上导致了免疫调节紊乱,从而参与了SLE的发病。     

CC chemokine receptor 4 expression on peripheral blood CD4+ T cells reflects disease activity of atopic dermatitis

Recent studies indicate that Th1 and Th2 cells differ in their chemokine receptor expression and their responsiveness to various chemokines. Therefore, selective Th2 cell recruitment in Th2-predominant inflammatory diseases such as atopic dermatitis may be under the influence of some chemokines. It is reported that CC chemokine receptor (CCR) 4 is selectively expressed on Th2 cells whereas CXC chemokine receptor (CXCR) 3 is selectively expressed on Th1 cells. In this study we examined CCR4 and CXCR3 expression on peripheral blood CD4+ and CD8+ T cells obtained from adult atopic dermatitis subjects, and compared the results with those from patients with psoriasis vulgaris and healthy controls. CCR4 was preferentially expressed on CD4+ T cells from atopic dermatitis subjects and CXCR3 was preferentially expressed on CD4+ T cells from psoriasis vulgaris subjects. This CCR4 expression was prominent especially in severe atopic dermatitis subjects. CCR4 expression on CD4+ T cells in severe atopic dermatitis subjects decreased on improvement of disease activity. CD25 was preferentially expressed on CCR4+CD4+ T cells but not on CXCR3+CD4+ T cells in atopic dermatitis subjects. Cutaneous lymphocyte-associated antigen was also preferentially expressed on CCR4+CD4+ T cells but not on CXCR3+CD4+ T cells in atopic dermatitis subjects. CD4+ T cells in atopic dermatitis skin lesions were predominantly CCR4+ cells. Taken together, this study strongly indicates that CCR4+CD4+ T cells reflect disease activity and suggests that CCR4 expression is important for T cell infiltration into atopic dermatitis lesions. Thus, CCR4 may be a possible target for therapy of atopic dermatitis in the future.     

High level of thymus and activation-regulated chemokine in blister fluid and sera of patients with bullous pemphigoid

BACKGROUND: Bullous pemphigoid (BP) is an autoimmune blistering disease characterized by eosinophilia and high serum IgE levels. The accumulated evidence suggests that various cytokines are involved in the lesional skin of patients with BP. Recently, thymus and activation-regulated chemokine (TARC/CCL17), a CC chemokine, was identified as a selective chemoattractant for CC chemokine receptor 4 (CCR4)-expressing cells. OBJECTIVE: In this study, we examined the involvement of TARC in patients with BP. METHODS: We determined the fluid and serum TARC levels in patients with BP by enzyme-linked immunosorbent assay and compared the serum TARC levels with the eosinophil numbers in peripheral blood. We also compared the serum TARC levels in five patients with BP before and after they were treated. Moreover, we examined TARC, CCR4 and CXC chemokine receptor 3 (CXCR3) expression in the lesional skin of patients with BP by immunohistochemical procedures. Furthermore, we measured CCR4 positivity in CD4+ CD45RO+ cells of peripheral blood mononuclear cells (PBMCs) in patients with BP and healthy control subjects. RESULTS: The fluid TARC levels in patients with BP were significantly higher than those in blisters from burn patients or suction blisters of healthy control subjects. The serum TARC levels in patients with BP were also significantly higher than those in pemphigus vulgaris (PV) patients and healthy control subjects, and decreased after the treatment. The serum TARC levels in patients with BP significantly correlated with the eosinophil numbers in peripheral blood (r = 0.72, P < 0.002). Immunohistochemistry showed a strong reactivity of TARC in the epidermal keratinocytes (KCs) of BP. Moreover, both CCR4 and CXCR3 were expressed on the dermal infiltrating CD4+ T cells mainly beneath the bullae of patients with BP. Fluorescence-activated cell sorting analysis showed a higher percentage of CCR4 positivity in CD4+ CD45RO+ cells of PBMCs in patients with BP than that in healthy control subjects, while there was no significant difference of CXCR3 positivity in CD4+ CD45RO+ cells of PBMCs between patients with BP and healthy control subjects. CONCLUSIONS: These findings strongly suggest that TARC may be one of the important chemokines that are involved in the pathogenesis of BP.     

Nickel-responding T cells are CD4+ CLA+ CD45RO+ and express chemokine receptors CXCR3, CCR4 and CCR10

BACKGROUND: Whereas T lymphocytes are widely accepted as effector cells determining the pathogenesis of allergic contact dermatitis, contradictory results have been found regarding the roles of different T-cell subsets. The use of various experimental models, involving long-term cultured T-cell lines or clones, may explain these contradictory results. OBJECTIVE: To investigate the involvement of distinct T-cell subsets in patients with nickel contact allergy. METHODS: Different T-cell subsets were directly isolated from peripheral blood mononuclear cells (PBMCs) of nickel-allergic patients, and their proliferative capacity, type-1 or type-2 cytokine secretion [measured by interferon (IFN)-gamma or interleukin (IL)-5 release] and phenotypical marker expression were analysed after stimulation with nickel. RESULTS: Only CD4+ CLA+ CD45RO+ and not CD8+ T cells proliferate and produce both type-1 (IFN-gamma) and type-2 (IL-5) cytokines in response to nickel. Moreover, cells expressing the marker CLA in combination with CD4, CD45RO or CD69 are increased after nickel-specific stimulation. Interestingly, in addition, CD45RA+ CLA+ cells showed an increased frequency after allergen-specific stimulation. Analysis of nickel-reactive T cells for expression of distinct chemokine receptors showed that both proliferative capacity and cytokine production are restricted to subsets expressing CXCR3, CCR4 but not CCR6. Fluorescence-activated cell sorting analysis of chemokine receptors expressed on nickel-stimulated T cells confirmed these results; a subset of T cells expressing CLA and CXCR3, CCR4 and, most importantly, CCR10 increased in response to allergen, while these CLA+ nickel-reactive T cells were all negative for CCR6. CONCLUSIONS: These findings demonstrate that freshly isolated nickel-reactive T cells can be characterized as CD4+ CLA+ memory T cells which express the chemokine receptors CXCR3, CCR4 and CCR10, but not CCR6.     

FS02.2CD4+ CCR10+ effector T cells reside at former allergic contact dermatitis sites

Local skin memory (LSM) describes the clinical phenomenon of an accelerated and increased inflammatory allergic contact dermatitis (ACD) response upon renewed allergen exposure. This has been ascribed to the local persistence of few, but allergen‐specific, T cells. Here, firstly, we characterized effector T cells, and, subsequently, studied which of these cell populations are present at former challenge sites and might contribute to LSM. Peripheral blood T cells were stimulated with nickel sulphate. Cellular phenotypes and chemokine receptor expression profiles were analysed by FACS‐staining: CLA together with CD4/CD8, CD45R0/RA, CXCR3, CCR4, CCR6 and CCR10. Skin biopsies were taken at 0, 3 and 21 days after allergen application and analysed for the same markers. Upon nickel‐stimulation, amount of CD4+ CLA+ CD45R0+ T cells was increased. Together with CLA, CXCR3, CCR4 and, mainly, CCR10 expression was augmented. CCR6 expression was negative on CLA+ cells. In biopsies from patch tests, cellular infiltrates were present at 3 and 21 days after allergen application. Interestingly at day 21, residing cells were localized at the perivascularity and were characterized as CD4+ CD8− CCR10+ T cells. In conclusion, nickel‐activated effector T cells can be characterised as CD4+ CD8− CLA+ memory T cells. They express CXCR3, CCR4 and, in particular, CCR10. After clinical recovery from an ACD reaction, CD4+ CCR10+ memory T cells apparently reside locally. The persistence of these CCR10+ T cells, expressing the appropriate receptor of the skin specific chemokine CCL27, can explain clinically important phenomena such as LSM and flare up reactions.     

Vitiligo with inflammatory raised borders, associated with atopic dermatitis

A 31-year-old man had had atopic dermatitis since childhood and developed vitiligo with inflammatory raised borders 5 years prior to presentation. Immunohistochemically, CD4+ T cells infiltrated predominantly in the raised border of vitiligo, while CD8+ T cells were present just outside of the borders, suggesting that CD8+ cells were an antecedent to the CD4+ cells. Despite the presence of atopic dermatitis, the percentage of CXCR3+ CD4+ Th1 cells increased in the patient's peripheral blood, compared with a representative atopic patient showing a high percentage of CCR4+CD4+ Th2 cells. This case suggests that vitiligo with inflammatory raised borders can occur even in patients with atopic dermatitis when Th1 cells are activated and overcome the Th2-dominant state.     

Homing receptor and chemokine receptor on intraepidermal T cells in psoriasis vulgaris

Intraepidermal T lymphocytes found in psoriatic skin lesions are involved in the development and maintenance of lesional pathology. It has become clear that differential expression of homing and chemokine receptors determines the specific migration of T cells to distinct tissues and microenvironments, including psoriasis lesions. The aim of the present study was to clarify expression of homing (CLA, VLA-4, and LFA-1) and chemokine (CCR4, CCR6, CCR7, and CXCR3) receptors on intraepidermal T cells in psoriatic lesions using flow cytometry. The vast majority of intraepidermal T cells in psoriatic lesions expressed CLA and LFA-1, whereas 58% of CD4+ and 85% of CD8+ T cells expressed VLA-4. The majority of CD4+ T cells and about half of the CD8+ T cells expressed CCR4 and CCR6, whereas less than one-third of CD4+ and CD8+ T cells expressed CXCR3 or CCR7. In patients with psoriasis the percentages of T cells expressing CLA, CCR4, and CCR6 were much higher in the epidermis of psoriatic plaques than in the peripheral blood. Thus, CLA, CCR4, and CCR6 may play a more important role in the migration of T cells to psoriatic epidermis.     

A Th2 chemokine, TARC, produced by keratinocytes may recruit CLA+CCR4+ lymphocytes into lesional atopic dermatitis skin

Atopic dermatitis is an inflammatory skin disease in which the inflammation is characterized by the influx of lymphocytes into the dermis. It is generally believed that atopic dermatitis is a Th2-type disease, i.e., the T lymphocytes produce interleukin-4, interleukin-5, interleukin-10, and interleukin-13, although it has become evident in recent years that the cytokine profile in the skin changes during the course of the disease towards a Th1-Th2 mixed cytokine profile (interferon-gamma, tumor necrosis factor alpha, and interleukin-2). The lymphocytes that home into the skin express cutaneous lymphocyte-associated antigen, and it has recently been shown that most of the lymphocytes in this population express the chemokine receptor CCR4. CCR4 is the receptor for the CC chemokine TARC (thymus and activation regulated chemokine), and this chemokine is expressed predominantly by keratinocytes in the basal layer of the epidermis of lesional atopic dermatitis skin in mice. In humans, however, it was shown to be expressed in the endothelial cells of the dermis. We have examined the peripheral blood mononuclear cells of atopic dermatitis patients for the expression of cutaneous lymphocyte-associated antigen and CCR4 and compared them with peripheral blood mononuclear cells from normal controls. We found that the proportion of CLA+CCR4+ lymphocytes is upregulated in atopic dermatitis patients. In addition we have examined skin biopsies of lesional and non-lesional skin from atopic dermatitis patients and found that the keratinocytes, but not the endothelial cells, produce TARC in the lesional but not in the nonlesional skin. To gain insight in the stimulatory mechanisms for TARC production in keratinocytes, as previously observed in mice, we cultured HaCaT cells and found that interferon-gamma and tumor necrosis factor alpha work synergistically to induce TARC production. These observations suggest that the induction of TARC production in keratinocytes plays an important role in the late phase skin invasion by CCR4+CLA+ Th2-type lymphocytes in atopic dermatitis.     

Lack of association of CCR4 single nucleotide polymorphism with atopic dermatitis in Japanese patients

CCR4, a member of the CC chemokine receptor family, is believed to play an important role in the pathogenesis of atopic dermatitis. To examine whether CCR4 single nucleotide polymorphism (SNP) is associated with susceptibility to atopic dermatitis, we investigated the allele and genotype frequencies of C1014T SNP of CCR4 in 198 Japanese patients with atopic dermatitis and controls by a PCR-restriction fragment length polymorphism method. There was no significant difference in allele or genotype frequencies between patients with atopic dermatitis and controls. Serum IgE levels and peripheral blood eosinophil counts were not significantly different among genotypes. There was also no significant difference in allele or genotype frequencies between the patient subgroup with and without asthma, with mild or moderate disease, with and without family history of atopic dermatitis, or with and without family history of atopic disorders. C1014T SNP of CCR4 does not appear to be associated with susceptibility to atopic dermatitis in Japanese patients.     

Circulating clonal CLA(+) and CD4(+) T cells in Sezary syndrome express the skin-homing chemokine receptors CCR4 and CCR10 as well as the lymph node-homing chemokine receptor CCR7

BACKGROUND: Adhesion molecules and chemokine receptors are involved in tissue-specific homing of T cells to the skin and play an important role in the pathophysiology of cutaneous lymphoma. It has recently been reported that the chemokine CCL27 expressed by keratinocytes attracts lymphocytes bearing the chemokine receptor CCR10. OBJECTIVES: To investigate the expression of CCR4, CCR7 and CCR10 on skin-homing CLA(+) and CD4(+) T cells in the peripheral blood of patients with Sezary syndrome (SS), a rare leukaemic variant of cutaneous T-cell lymphoma. METHODS: Lymphocytes from five patients with SS, six patients with mycosis fungoides and four healthy volunteers were isolated and analysed using flow cytometry. Additionally, the T-cell receptor (TCR)-Vbeta CDR3 regions were cloned and sequenced in two patients. RESULTS: We found that CCR4 is expressed on almost all CLA(+) and CD4(+) memory T cells. Using monoclonal antibodies specific for single TCR-Vbeta chains we identified malignant T cells in four patients with SS. Importantly, we found that most but not all malignant Sezary cells expressed the skin-homing chemokine receptor CCR10. Additionally, we found that a significant proportion of these cells also expressed the lymph node-homing chemokine receptor CCR7. CONCLUSIONS: Our results support the concept that chemokine receptors play an important role in the pathophysiology of SS and suggest that the malignant clone may represent an expansion of skin-homing cutaneous 'central' memory T cells in the peripheral blood of these patients.