Leptin enhances availability of apoptotic cell-derived self-antigen in systemic lupus erythematosus

In systemic lupus erythematosus (SLE), the availability of self-antigen promotes and fuels self-reactive immune responses. Apoptotic cells represent a major source of self-antigens, and an impairment of the removal of apoptotic material containing self-antigen can contribute to the development of autoimmunity. To address whether the adipocytokine leptin--which favors autoimmune responses through little understood mechanisms--could modulate the handling of apoptotic cells in SLE, we evaluated the ability of leptin to modulate the capacity of macrophages to phagocytose apoptotic bodies in (NZB × NZW)F1 lupus mice. It was found that leptin promoted phagocytosis of apoptotic cells by macrophages by modulating cAMP levels in macrophages. This finding associated with an increased availability of antigen that favored the development of T cell responses to apoptotic-derived antigen. As leptin promotes macrophage phagocytosis of apoptotic bodies in SLE and subsequent availability of apoptotic-derived antigen to T cells, an inhibition of this process via leptin blockade might have a therapeutic potential in SLE

Leptin enhances availability of apoptotic cell-derived self-antigen in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE), the availability of self-antigen promotes and fuels self-reactive immune responses. Apoptotic cells represent a major source of self-antigens, and an impairment of the removal of apoptotic material containing self-antigen can contribute to the development of autoimmunity. To address whether the adipocytokine leptin--which favors autoimmune responses through little understood mechanisms--could modulate the handling of apoptotic cells in SLE, we evaluated the ability of leptin to modulate the capacity of macrophages to phagocytose apoptotic bodies in (NZB × NZW)F1 lupus mice. It was found that leptin promoted phagocytosis of apoptotic cells by macrophages by modulating cAMP levels in macrophages. This finding associated with an increased availability of antigen that favored the development of T cell responses to apoptotic-derived antigen. As leptin promotes macrophage phagocytosis of apoptotic bodies in SLE and subsequent availability of apoptotic-derived antigen to T cells, an inhibition of this process via leptin blockade might have a therapeutic potential in SLE

Leptin enhances availability of apoptotic cell-derived self-antigen in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE), the availability of self-antigen promotes and fuels self-reactive immune responses. Apoptotic cells represent a major source of self-antigens, and an impairment of the removal of apoptotic material containing self-antigen can contribute to the development of autoimmunity. To address whether the adipocytokine leptin--which favors autoimmune responses through little understood mechanisms--could modulate the handling of apoptotic cells in SLE, we evaluated the ability of leptin to modulate the capacity of macrophages to phagocytose apoptotic bodies in (NZB × NZW)F1 lupus mice. It was found that leptin promoted phagocytosis of apoptotic cells by macrophages by modulating cAMP levels in macrophages. This finding associated with an increased availability of antigen that favored the development of T cell responses to apoptotic-derived antigen. As leptin promotes macrophage phagocytosis of apoptotic bodies in SLE and subsequent availability of apoptotic-derived antigen to T cells, an inhibition of this process via leptin blockade might have a therapeutic potential in SLE

Comics as an educational tool for children with juvenile idiopathic arthritis

Abstract Background This study examined whether the comic book Neta and the Medikidz Explain JIA would improve disease-related knowledge and treatment adherence among patients with juvenile idiopathic arthritis (JIA). Methods In this prospective cohort study, JIA patients answered 20 multiple-choice knowledge questions about their disease, before and after reading the comic book. Demographic, clinical, health-related quality of life and adherence data were recorded and correlated to the responses. Results We studied 61 patients with a mean age of 14 ± 3.3 (range 8–18) years, 67% female, 83% Jewish and 17% non-Jewish. Thirty-nine percent had oligoarthritis, 13% systemic, 32% polyarthritis 11% psoriatic and 5% enthesitis-related type JIA. The disease was active in 46%, 40% were treated with biologics/disease modifying anti-rheumatic drugs, and 34% were in remission on medication. Among the 53 patients who completed before and after quizzes, average score increased from 63 to 80% (P < 0.001). Non-Jewish patients initially scored lower than Jewish patients (48%), but their score increased to 79% after reading the comic book. Twenty-seven patients who also completed the quiz 1 year after the first reading retained their knowledge (79%). We did not find a statistically significant correlation between knowledge and age, sex, disease subtype, or Child Health Questionnaire quality of life scores. Adherence to medication use, physical therapy and rheumatology clinic visits were high at baseline; thus, these did not change after reading the comic. Conclusions The comic booklet Neta and the Medikidz Explain JIA is a good educational tool for increasing disease-related knowledge in children with JIA

Increased macrophage uptake of apoptotic cells induced by leptin promotes proliferation of self antigen-reactive T cells.

<p>TAMRA-labeled apoptotic bodies containing OVA (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0112826#s2" target="_blank">Methods</a>) were co-cultured with CFSE-labeled macrophages for 2 h, followed by staining with APC-labeled anti-CD11b Ab and flow cytometry. (A) Frequency of TAMRA⁺CFSE⁺ CD11b⁺ cells (macrophages positive for OVA-containing apoptotic bodies) in OVA-TCR transgenic mice (DO11.10) after culture in the presence of scalar doses of leptin. (B) Flow cytometry staining with clonotype-specific KJ1.26 Ab (OVA-specific TCR) 48 h after co-incubation of OVA-immunized DO11.10 (OVA-TCR transgenic) mouse splenocytes with macrophages containing OVA-loaded apoptotic bodies (TAMRA⁺). *p<0.05, **p<0.01 vs control (n = 5).</p