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Printable Handouts
Navigable Slide Index
- Introduction
- Contents
- Innate Lymphoid Cells (ILCs)
- Cytokine producing lymphocytes
- Differentiation pathways of ILCs
- ILC classification
- Allergic diseases and ILCs
- Helminth infection and allergic inflammation
- Adaptive immunity against helminths and allergens
- Identification of ILC2
- IL-33 and IL2 + IL-25
- Epithelial cell-derived IL-33 and IL-25 (1)
- Epithelial cell-derived IL-33 and IL-25 (2)
- Innate immunity against helminths and allergens
- Role of ILC2 in allergic diseases
- Lung inflammation by papain
- Papain treatment
- Intratracheal administration of IL-33 or IL-2 + IL-25 induces eosinophilia in the lung
- Lung eosinophilia
- ILC2 are tissue-resident cells
- TSLP-STAT5 axis in corticosteroid sensitivity of ILC2 cells
- Steroid-resistant severe asthma and ILC2
- Dexamethasone suppresses IL-33-induced inflammation in the lung
- Dexamethasone suppresses OVA-induced inflammation in the lung
- Dexamethasone is unable to suppresses OVA-induced inflammation in the presence of IL-33
- Difference in the sensitivity between T cells and ILC2 cells
- Dexamethasone suppresses the proliferation of ILC2 and induces apoptosis of ILC2 in vitro
- IL-2, IL-7 and TSLP antagonize corticosteroid sensitivity of ILC2
- TSLP antagonizes the effect of corticosteroid on NH (ILC2) cells
- Neutralization of TSLP antagonizes corticosteroid resistance in vivo
- STAT5 inhibitors suppress the effect of TSLP
- STAT5 inhibitors restore corticosteroid sensitivity
- Role of ILC2: summary
- Clinical significance of TSLP
- How is the type 2 inflammatory response terminated?
- IFNs strongly suppress proliferation of ILC2
- IFNs strongly suppress cytokine production by ILC2
- IFNγ suppresses airway hyperreactivity
- IFNγ suppresses ILC2 activation during inflammation
- Mechanisms
- Interferon-γ and IL-27
- A cytokine-mediated balance of ILC functions
- Factors affecting ILC2 functions
- Clinical significance of interferons
- Clinical significance of type 1 cytokines
- Role of other ILCs in allergic diseases
- Conclusion
- Thank you for your attention!
Topics Covered
- Innate Lymphoid Cells (ILCs)
- Allergy and ILCs
- Type 1 and 2 cytokine responses
- Innate and adaptive immunity
- Asthma
- Lung eosinophilia
- Mucus secretion
- Helminth infection and allergic inflammation
- Epithelial cell-derived IL-33 and IL-25
- Lung inflammation by papain
- TSLP-STAT5 axis
- Corticosteroid sensitivity
- Interferons (IFNs) and ILCs
Links
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Therapeutic Areas:
Talk Citation
Koyasu, S. (2024, February 29). Innate lymphoid cells in allergy [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 21, 2024, from https://doi.org/10.69645/KQIJ2045.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Emeritus Shigeo Koyasu has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Other Talks in the Series: The Immune System - Key Concepts and Questions
Other Talks in the Series: Allergy - From Basics to Clinic
Transcript
Please wait while the transcript is being prepared...
0:00
Hello, my name is Shigeo
Koyasu from Keio University.
I'll talk about the
innate lymphoid cells
in allergic diseases.
0:10
So, the contents
are in five rows.
I'll start with what innate
lymphoid cells (ILCs) are and
then an overview about the
allergic diseases and ILCs.
Then, I'll talk
about the role of
ILC2 in allergic diseases
with our own data.
I'll briefly mention about
the role of other ILCs
in allergic diseases and
then, I'll conclude my talk.
0:36
So, what are ILCs?
ILCs are lymphocytes without
Rag-dependent rearranged
antigen receptors.
So, they don't have
any antigen receptors.
The first innate lymphoid
cells discovered
was natural killer (NK) cells
that were found in 1975,
and the next one was
lymphoid tissue inducer
(LTi) cells found in 1997,
which plays a role during
the fetal stages to
induce lymph nodes and
Peyer's patches, and so on.
Those are the so-called
first-generation
innate lymphoid cells,
1:16
but in 21st century,
we found three new types
of innate lymphoid cells.
We know that there are three
types of helper T-cells,
Th1, Th17,
and Th2 with T-cell receptors.
Th1 cells produce
interferon-gamma (IFNγ),
which act on macrophages (Mϕ)
and then act on fighting
against the intracellular
microbes and viruses.
Th17 cells produce IL-17 and
IL-22 which mostly act
on epithelial cells,
which plays an important
role for immunity against
fungi and Escherichia bacteria,
such as EHEC and ETEC.
Th2 cells producing
IL-5 and IL-13
induce eosinophilia and
goblet cell hyperplasia,
which play an important role
in immunity against helminth.
Those are in adaptive
immunity, but
during the innate immune
phase, as I said,
NK cells was found in 1975,
which are able to produce
IFNγ as Th1 cells.
Around 2008-2009, people
found LTi-like cells in
adult intestine which do
not have T-cell
receptors, but are
able to produce IL-17 and
IL-22 as Th-17 cells.
Next, innate lymphocytes
they found was
the T-bet^+ EOMES^-
innate lymphocytes,
which are able to produce IFNγ,
but possess very low
level of cytotoxicity.
So, therefore, we now know
that NK cells correspond to
CTL (cytotoxic lymphocytes) and
T-bet^+ EOMES^- cells
correspond to Th1 cells.
Lastly, natural helper
cells, which we named,
expressing GATA3 was discovered,
which again lack T-cell
receptors, but are
able to produce IL-5
and IL-13 as Th2 cells.
So, pros for those cells
are they actually play
an important role for immunity
against various
invading microbes,
fungi, and helminths,
but cons are they
induce various types of acute
and chronic inflammation.
In 2013, people working in
this field decided to
call γ producers as
Group 1 ILC or ILC1,
type 2 cytokine producing cells
Group 2 ILCs or ILC2,
and IL-17,
IL-22 producing cells as
Group 3 ILCs or ILC3.