• Users Online: 149
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
REVIEW ARTICLE
Year : 2019  |  Volume : 3  |  Issue : 1  |  Page : 3-7

Complements and allergic asthma


1 Clinical Immunology Center, China Medical University, Children's Hospital, Taichung, Taiwan
2 Department of Pediatrics, Changhua Christian Hospital Children's Hospital, Changhua, Taiwan

Correspondence Address:
Ching-Yuang Lin
Clinical Immunology Center, China Medical University, Children's Hospital, No. 2, Yun-Der Road, Taichung 40402
Taiwan
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/prcm.prcm_5_18

Rights and Permissions

Regulatory T (Treg) cells play a central role in protecting against the development of allergic asthma and interleukin-10 (IL-10) producing T regulatory type 1 (Tr1) cells contribute to the regulation of asthma. Complement regulatory protein CD46 was shown to stimulate the development of IL-10 producing Tr1 cells. Crosslinking of CD46 during CD4+ T cell priming induces production of large amount of IL-10 and granzyme B. These CD46-induced regulatory T cells (Tr1) does not require pre-existing basal expression of FoxP3. Through local IL-10 and granzyme B secretion, such Tr1 cell could control T-cell-mediated inflammation. In asthmatic patients, we found that diminished IL-10, granzyme B, and CCR 4 expression from CD3/CD46-activated Tr1 cells. CD3/CD46-activated Tr1 cells from asthma patients co-cultured with BEAS-2B cells suppressed dermatophagoides pteronyssinus 2 (Der p 2)-induced nuclear factor-κB/p65 by cell contact inhibition. Decreased interaction of CD3/CD46-activated Tr1 and BEAS-2B cells from asthmatics was associated with downregulation of phosphorylation of protein kinase B expression. Decreased interaction between CD46-mediated Tr1 and lung epithelial cells with less IL-10 and granzyme B production may contribute to airway inflammation in allergic asthma. Der p specific immunotherapy enhances the suppressive function of IL-10 in CD46-mediated Tr1 cell from asthmatic patients and suppresses airway inflammation in these patients. Based on these results, it might be possible to design therapeutic strategies to manipulate complement activated Tr1 cells to achieve allergen tolerance and suppress airway inflammation in patients with allergic asthma.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed106    
    Printed8    
    Emailed0    
    PDF Downloaded10    
    Comments [Add]    

Recommend this journal