Download 20150923_koyasu

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts

Sociality and disease transmission wikipedia, lookup

T cell wikipedia, lookup

Infection wikipedia, lookup

Hospital-acquired infection wikipedia, lookup

Social immunity wikipedia, lookup

Lymphopoiesis wikipedia, lookup

Neonatal infection wikipedia, lookup

Phagocyte wikipedia, lookup

Molecular mimicry wikipedia, lookup

Sjögren syndrome wikipedia, lookup

Infection control wikipedia, lookup

Autoimmunity wikipedia, lookup

DNA vaccination wikipedia, lookup

Inflammation wikipedia, lookup

Adoptive cell transfer wikipedia, lookup

Polyclonal B cell response wikipedia, lookup

Cancer immunotherapy wikipedia, lookup

Immune system wikipedia, lookup

Adaptive immune system wikipedia, lookup

Allergy wikipedia, lookup

Immunosuppressive drug wikipedia, lookup

Innate immune system wikipedia, lookup

Immunomics wikipedia, lookup

Hygiene hypothesis wikipedia, lookup

Psychoneuroimmunology wikipedia, lookup

Transcript
Regulation of ILC2 activities in allergic
inflammation
September 22(Tue), 11:00 / Auditorium (1F), PBC
Shigeo Koyasu
RIKEN Center for Integrative Medical Sciences, Keio University School of Medicine
The type 2 immune response, characterized by the production of
IL-4, IL-5 and IL-13, is a critical immune response against helminths
invading cutaneous or mucosal sites. In addition, type 2 immune
responses are involved in the pathophysiology of various allergic
diseases including asthma. Type 2 cytokines are induced soon after
helminth infection or certain allergic responses such as papaininduced airway inflammation even before an antigen-specific
adaptive immune response is established. We have identified a
previously unidentified lymphocyte population producing large
amounts of type 2 cytokines, which we named Natural helper (NH)
cells and are now a member of group 2 innate lymphoid cells
(ILC2s). We identified ILC2s in lymphoid clusters in adipose tissues,
which we termed fat-associated lymphoid cluster (FALC). ILC2s
produce type 2 cytokines constitutively without any stimulation,
and support the self-renewal of B1 cells and IgA production by B
cells. Stimulation by IL-33 or helminth infection activates ILC2s to
produce large amounts of IL-5 and IL-13, which induce eosinophilia
and goblet cell hyperplasia, both of which play an important role in
anti-helminth immunity and pathophysiology of allergic diseases.
We have recently found that IFNγ and IL-27 suppress tissueresident ILC2s that expand in situ without migration during
helminth infection and fungi infection in a STAT1-dependent
manner. ILC2-mediated lung inflammation was enhanced in the
absence of IFNγ receptor signals in vivo. Our results suggest that
IFNγ- and IL-27-mediated suppression of tissue-resident ILC2s is a
negative feedback mechanism for ILC2 functions in vivo.
Inquiry: AIM Administrative Team (Tel.279-8628, E-mail: [email protected])