International Immunology 2009 21(5):NP; doi:10.1093/intimm/dxp040
© The Japanese Society for Immunology. 2009. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org
IN THIS ISSUE
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Differentiation and functions of Th17 cells in inflammation
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In this review,
Awasthi and Kuchroo (p. 489) outline the discovery
of T
h17 cells and detail recent findings about the interplay
between T
h17 cells and regulatory T cells. The authors describe
how T
h17 responses are amplified and negatively regulated, highlighting
the role of T
h17-specific transcription factors. Finally they
discuss how human T
h17 cells function in inflammation and infection.
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Non-MHC autoimmune modifier loci in NOD mice
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Nonobese diabetic (NOD) mice are prone to several organ-specific
and non-organ-specific autoimmune diseases in addition to type
1 diabetes.
Honjo and colleagues (p. 499) identify several non-MHC
quantitative trait loci (QTL) for these diseases; however, some
diabetes QTL overlapped and could protect against or promote
other autoimmune diseases. The results will help identify modifier
genes that regulate autoimmunity.
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Peritoneal factors control arthritis susceptibility
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BALB/c mice are susceptible to intraperitoneal proteoglycan
aggrecan induced arthritis (PGIA). Here,
Glant and colleagues (p. 511) show that resident peritoneal B1 cells are replaced
by conventional B cells and T cells; the latter produce IFN-
and IL-17. The peritoneal cells can transfer disease, and the
authors propose that these T cells can "switch" susceptibility
to rheumatoid arthritis.
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Characterization of CCR4+CD8+ cells
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Kondo and Takiguchi (p. 523) characterise the human C–C
chemokine receptor 4 (CCR4)
+CD8
+ subset and suggest that it
comprises immature memory cells that can secrete T
h1 and T
h2
cytokines. Like memory T
h2 cells, CCR4
+CD8
+ cells appear to
home to skin. The authors suggest CCR4 as a useful marker for
diseases such as atopic dermatitis.
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Enhanced immunoglobulin binding to NOD B cells
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Lejon and colleagues (p. 533) describe a novel immunoglobulin-receptor
that is intrinsically present on B6 B cells but is more abundant
in nonobese diabetic (NOD) mice. Consequently, all peripheral
NOD B cells carry extramembranous IgG and IgM and bind more
immune complexes. The authors propose that the receptor functions
in normal immune responses but might contribute to autoimmune
disease.
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Lipid hydrolysis in CTL-mediated killing
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Using various experimental approaches,
Alves et al. (p. 543) show that fatty acids are released from dying targets but this
release appears to be independent of CTL lipase activity; lipase
inhibitors block fatty acid release but do not block CTL-mediated
killing. The authors discuss the contribution of target-cell
lipases and the consequences of the release of target-cell fatty
acids.
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IL-17A and IL-22 production early in salmonellosis
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In this article,
Alber and colleagues (p. 555) characterise
the production of IL-22 and IL-17A after intraperitoneal infection
with
Salmonella enterica serovar Enteritidis. IL-22 responses
peak earlier, are sustained in serum and are IL-23-dependent.
Dendritic cells initiate IL-22 production whereas
T cells are
an important source of IL-17A. These cytokines are therefore
differentially regulated early in infection.
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TGF-β is required for the function, not induction, of CD8+ Tregs
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Injecting antigen into the anterior chamber of the eye induces
splenic CD8
+ regulatory T cells (T
regs) that suppress delayed-type
hypersensitivity (DTH) responses; similar T
regs are generated
after
in vitro exposure to transforming growth factor β
(TGF-β). In the
in vivo system,
Cone et al. (p. 567) show
that TGF-β appears non-essential for T
reg induction, but
that suppression of DTH does require TGF-β.
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Phosphorylation of c-Abl early in B cell development
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The proto-oncogene c-Abl is a src-family kinase known to be
important for B cell maturation and leukemic transformation.
Brightbill and Schlissel (p. 575) find that large amounts of
IL-7 can rescue defects caused by aberrant c-Abl expression.
Additionally, they show that c-Abl phosphorylation peaks at
the early pro-B cell stage.
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FasL can inhibit T cell activation
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Using freshly isolated human T cells,
Janssen and colleagues (p. 587) cross-link Fas ligand (FasL) with antibodies or fusion
proteins, and thereby inhibit signalling and proliferation triggered
by TCR plus CD28 stimulation; addition of IL-2 cannot reverse
this effect. The authors also describe the effects on protein
phosphorylation. The results imply an important cross-talk between
TCR and FasL signalling pathways.
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NK cells upregulate membrane-bound IL-15 on DCs
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NK cells are known to activate dendritic cells (DCs) by secreting
IL-12. Here,
Ferlazzo and colleagues (p. 599) show that, after
recognising class I deficient cells, NK cells secrete cytokines
that upregulate membrane-bound IL-15 on DCs; only some of this
IL-15 associates with IL-15R
. The IL-15 is crucial for activation
of antigen-specific T cells if IL-12 is absent.
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Inhibition of RNA-dependent TLR stimulation
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Foreign nucleic acids are important ligands for Toll-like receptors
(TLRs).
Vollmer and colleagues (p. 607) demonstrate that 2'-O-methylation
at various positions of self RNA strongly interferes with recognition
by TLRs, independently of the position of the modified nucleotide.
The authors discuss how RNA modification and the intracellular
location of such RNA affect self recognition and immune regulation.
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Differentiation and functions of...
Non-MHC autoimmune modifier loci...