Skip to main content
Article thumbnail
Location of Repository

IL-32: An Emerging Player in the Immune Response Network against Tuberculosis?

By Manikuntala Kundu and Joyoti Basu


IL-32 has emerged as an important player in innate and adaptive immune responses. Kundu and Basu discuss a new study in PLoS Medicine that explored the role of IL-32 in the context of M. tuberculosis infection

Topics: Perspectives
Publisher: Public Library of Science
OAI identifier:
Provided by: PubMed Central
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://www.pubmedcentral.nih.g... (external link)
  • Suggested articles


    1. Ding A (2006) MyD88-mediated stabilization of interferon-γ-induced cytokine and chemokine mRNA.
    2. (2004). Fatal Mycobacterium tuberculosis infection despite adaptive immune response in the absence of MyD88.
    3. (2006). Genetic analysis of host resistance: Toll-like receptor signalling and immunity at large.
    4. (2005). IL-32 synergizes with nucleotide oligomerization domain (NOD) and NOD2 ligands for IL-1β and IL-6 production through a caspase 1-dependent mechanism.
    5. (2006). IL-32, a proinfl ammatory cytokine in rheumatoid arthritis.
    6. (2002). Inherited disorders of IL-12- and IFNγ-mediated immunity: A molecular genetics update.
    7. (2005). Interleukin-32: A cytokine and inducer of TNFα.
    8. (2006). Mycobacterium tuberculosis induces interleukin-32 production through a caspase-1/IL-18/interferon-γ dependent mechanism. PLoS Med 3: In press.
    9. (2005). NOD-LRR proteins: Role in host-microbial interactions and infl ammatory disease.
    10. (2005). NOD2 and Tolllike receptors are nonredundant recognition systems of Mycobacterium tuberculosis .
    11. (2002). Pulmonary miliary tuberculosis in a patient with anti-TNF-alpha treatment.
    12. (2003). Translational control by the 3′-UTR: The ends specify the means.

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.