Indexado em
  • Abra o Portão J
  • Genamics JournalSeek
  • CiteFactor
  • cosmos SE
  • Scimago
  • Diretório de Periódicos de Ulrich
  • Biblioteca de periódicos eletrônicos
  • RefSeek
  • Universidade de Hamdard
  • EBSCO AZ
  • Diretório de Indexação de Resumos para Periódicos
  • OCLC- WorldCat
  • Invocação Proquest
  • Scholarsteer
  • ESTRADA
  • Biblioteca Virtual de Biologia (vifabio)
  • publons
  • Fundação de Genebra para Educação e Pesquisa Médica
  • Google Scholar
Compartilhe esta página
Folheto de jornal
Flyer image

Abstrato

Doe s intrinsic immune defect against common microbial pathogen s play an important role in arthritic manifestation?

*S Subramanian, S Dhivya

The autoimmune diseases are characterized by inflammation and resulting degradation of macromolecules of specific foci. Etiopathogenesis of arthritis is still unclear. In recent times many studies have been published, giving satisfactory explanation of infection and defective immune mechanisms for arthritic etio-pathogenesis. Understanding etio-pathogenesis is the most important and fundamental aspect of any particular problem. Many have given their different views on the above to educate the society. Out of these views, very few clear views were brought to the notice on immune dysfunction to common microbial infections. Convincingly, the above may have a strong connection to the disorder. Generally, it is thought that common microbial infections cause known problems but in unforeseen situation the dysregulation of immune function may also have acceptable reason behind the etio-pathogenesis. Vice-versa, defective immune functions like defective B cell function, defective B Cell Receptor signaling mechanism, dysregulated cytokine function, auto-antibodies’ cross reactivity to self antigens, inappropriate complement cascade events and defective apoptosis are few privileged environments which are discussed here for possible explanation of etiology of rheumatoid arthritis. This review deals with infection connection and defective immune mechanism of rheumatoid manifestation for further better understanding of etiopathogenesis.

Isenção de responsabilidade: Este resumo foi traduzido usando ferramentas de inteligência artificial e ainda não foi revisado ou verificado