Immunodeficiency in the lupus clinic

Karim, Mohammed Yousuf

doi:10.1191/0961203306lu2282rr

Cited by 11 publications

(4 citation statements)

References 23 publications

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“…This hypothesis is confirmed in a study by Lu et al [22], who report that methylprednisolone inhibits the survival of activated CD4 + lymphocytes activated by specific TLR3 and TLR9 ligands in vitro but has no effect on their expression. What is more, immunosuppressive therapy leads to hypogammaglobulinemia and secondarily induces immune deficiency [23]. There were 8 subjects (23%) with hypogammaglobulinemia in our group and half of them were receiving immunosuppressants.…”

Section: Discussionmentioning

confidence: 85%

Expression of Toll-Like Receptors 3, 7, and 9 in Peripheral Blood Mononuclear Cells from Patients with Systemic Lupus Erythematosus

Klonowska-Szymczyk

Wolska

Robak

et al. 2014

Mediators of Inflammation

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Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown aetiology. The results of experimental studies point to the involvement of innate immunity receptors—toll-like receptors (TLR)—in the pathogenesis of the disease. The aim of the study was to assess the expression of TLR3, 7, and 9 in the population of peripheral blood mononuclear cells (PBMC) and in B lymphocytes (CD19+), T lymphocytes (CD4+ and CD8+) using flow cytometry. The study group included 35 patients with SLE and 15 healthy controls. The patient group presented a significantly higher percentage of TLR3- and TLR9-positive cells among all PBMCs and their subpopulations (CD3+, CD4+, CD8+, and CD19+ lymphocytes) as well as TLR7 in CD19+ B-lymphocytes, compared to the control group. There was no correlation between the expression of all studied TLRs and the disease activity according to the SLAM scale, and the degree of organ damage according to the SLICC/ACR Damage Index. However, a correlation was observed between the percentage of various TLR-positive cells and some clinical (joint lesions) and laboratory (lymphopenia, hypogammaglobulinemia, anaemia, and higher ESR) features and menopause in women. The results of the study suggest that TLR3, 7, and 9 play a role in the pathogenesis of SLE and have an impact on organ involvement in SLE.

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Section: Discussionmentioning

confidence: 85%

Expression of Toll-Like Receptors 3, 7, and 9 in Peripheral Blood Mononuclear Cells from Patients with Systemic Lupus Erythematosus

Klonowska-Szymczyk

Wolska

Robak

et al. 2014

Mediators of Inflammation

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“…Based on the frequency of associations with autoimmune diseases, PIDs can be grouped in three groups, as follows: systematic (Ͼ80% of the patients with the disorder have autoimmune disease symptoms), strong (20 -80%), and mild (Ͻ20% of the patients) and absent (12,57). Some PID patients appear susceptible also to atopy and lupus-like syndromes (58).…”

Section: Parameters Characterizing Primary Immunodeficienciesmentioning

confidence: 99%

Systematic Classification of Primary Immunodeficiencies Based on Clinical, Pathological, and Laboratory Parameters

Samarghitean

Ortutay²,

Vihinen

2009

The Journal of Immunology

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The classification of diseases has several important applications ranging from diagnosis and choice of treatment to demographics. To date, classifications have been successfully created manually, often within international consortia. Some groups of diseases, such as primary immunodeficiencies (PIDs), are especially hard to nosologically cluster due, on one hand, to the presence of a wide variety of disorders and, in contrast, because of overlapping characteristics. More than 200 PIDs affecting components of the innate and adaptive immune systems have been described. Clinical, pathological, and laboratory characteristics were collected and used to group PIDs. A consensus of at least five independent methods provided a novel classification of 11 groups, which revealed previously unknown features and relationships of PIDs. Comparison of the classification to independent features, including the severity and therapy of the diseases, functional classification of proteins, and network vulnerability, indicated a strong statistical support. The method can be applied to any group of diseases.

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“…Scattered reports of transient or permanent hypogammaglobulinemia with an increased risk of infections were informed prior to the use of anti-CD20 therapies. Alternatively, many patients with SLE display a prominent polyclonal B-cell activation and hypergammaglobulinemia (Yong et al, 2008, Karim 2006Battafarano et al 1998). Transient or permanent spleen dysfunction is associated with diverse autoimmune diseases including SLE.…”

Section: Cellular Immune Defectsmentioning

confidence: 99%