earticle

논문검색

Poster-15

The Role of a C-type Lectin, SIGN-R1, in The Supression of Autoimmune Disease by IVIG

원문정보

초록

영어

The intricate system of serum complement proteins provides resistance to infection. The spleen and complement C3 provide resistance against blood-borne S. pneumoniae infection. To better understand the mechanisms involved, we studied SIGN-R1, a lectin that captures microbial polysaccharides in spleen marginal zone. We found that SIGN-R1 directly bound the complement C1 subcomponent, C1q, and assembled a C3 convertase, but without the traditional requirement for either antibody or factor B. Therefore the transmembrane lectin SIGN-R1 contributes to innate resistance by an unusual C3 activation pathway, unraveling the novel and 4th complement activation pathway (1) It has been reported that sialylation on Fc doamin of immunogloublin is critical for the effect of intravenous immunoglobulin (IVIG) and seems to be mediated by lectins which are expressed on splenic marginal zone macrophages (2,3). And they demonstrated that SIGN-R1 preferentially binds to 2,6-sialylated Fc compared with similarly sialylated, biantennary glycoproteins, thus suggesting that a specific binding site is created by the sialylation of IgG Fc (4). Moreover, they showed that a human homologue of SIGN-R1, DC-SIGN, displays a similar binding specificity to SIGN-R1 but differs in its cellular distribution, potentially accounting for some of the species differences observed in IVIG protection (5). However, the function of DC-SIGN in IVIG effects is controversial now, given that DC-SIGN and alpha2,6-sialylated IgG Fc interaction is dispensable for the anti-inflammatory activity of IVIg on human dendritic cells (6). Autoantibody is the principal mediators of autoimmune disease. IVIG is a milestone of the therapy of autoimmune disease. Now we hypothesize that complement systems are essential for the recognition of the sialylated Fc domain of immunoglobulin by SIGN-R1 or DC-SIGN, which lead to various IVIG effects or anti-inflammatory effects. In our further studies, we hope to further characterize the SIGN-R1-mediated IVIG effects and these works could lead to develop a potential therapeutic target against several autoimmune diseases.

저자정보

  • Young Sun Kang Dept. Biomedical Science & Technology, Institute of Biomedical Science & Technology (IBST), Laboratory of innate immunity, Konkuk University

참고문헌

자료제공 : 네이버학술정보

    함께 이용한 논문

      ※ 원문제공기관과의 협약기간이 종료되어 열람이 제한될 수 있습니다.

      0개의 논문이 장바구니에 담겼습니다.