International Immunology 2008 20(10):NP; doi:10.1093/intimm/dxn107
© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org
IN THIS ISSUE
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Complement peptide inhibits mast cell responses
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Complement components can activate certain mast cell functions.
Here,
Erdei and colleagues (p. 1239) show that C3a9 —
a peptide derived from C3a — binds mast cell Fc
RI–IgE
complexes, affecting receptor internalisation and the phosphorylation
of various kinases; it also affects cytokine secretion. This
fragment therefore inhibits both the immediate and late-phase
responses of mast cells.
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Different TCR–CD3 structures on CD4+ and CD8+ cells
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Previously,
Regueiro and colleagues (p. 1247) showed that antibodies
can distinguish the
βTCR–CD3 complex on human CD4
+ versus CD8
+ T cells. The authors now show a similar phenomenon
in seven other mammalian species. The effect appears to be due
to differential glycosylation. These findings are interesting
for phylogenetic studies, but also have important implications
for clinical immunology.
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DC-STAMP regulates autoimmunity and DC function
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Although originally identified in dendritic cells (DCs), the
role of DC-specific transmembrane protein (DC-STAMP) in these
cells is unclear.
Miyamoto and colleagues (p. 1259) show that
aged DC-STAMP-deficient mice show several symptoms of autoimmunity.
The deficient DCs show increased phagocytic activity and thus
increased antigen presentation; the authors describe the implications
for DC function and autoimmunity.
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A new model for T helper subset differentiation
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Existing mathematical models of T
h1/T
h2 differentiation cannot
easily accommodate new phenotypes such as T
h17 cells. In this
article,
van den Ham et al. (p. 1269) describe a new model that
includes ‘master regulators’, in particular transcription
factors such as GATA3 and FoxP3; the model can incorporate novel
regulators/phenotypes that are discovered, and applies to non-immunological
systems.
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Fas expression and germinal centre tolerance induction
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Apoptosis plays a role in tolerance induction during the germinal
centre (GC) reaction.
Manser and colleagues (p. 1279) show that
B cell Fas deficiency does not rescue participation of a test
clonotype in the GC reaction; notably, transfer of Fas-sufficient
clonotypes to Fas-deficient hosts reduces clonotype participation
in the reaction. The authors discuss potential roles of Fas-ligand,
and implications for tolerance.
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Selective role of Gads in allergy
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Using Gads–/– mice,
Yamasaki et al. (p. 1289) show
defective mast cell responses to Fc
RI crosslinking and impaired
in vivo allergic responses. Mast cell responses to bacterial
infection appear unaffected, as do various B and T cell responses.
The authors therefore speculate that the adaptor protein Gads
might be a selective target for control of allergic responses.
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Altered immunity in D4-GDI transgenic mice
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D4-GDI inhibits GDP dissociation from Rho-family members. Here,
Kondoh et al. (p. 1299) used transgenic mouse T cells to examine
a mutated D4-GDI found in human leukemic cells.
In vitro, the
mutation enhances T cell proliferation and cytoskeletal organisation;
in vivo granuloma formation in response to bacillus Calmette–Guérin
and host survival after
Listeria infection are improved.
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Glatiramer acetate has little effect in lupus
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Glatiramer acetate (GA) is approved as therapy for multiple
sclerosis and there is speculation that it might also be effective
in many other autoimmune diseases. After thoroughly examining
the effects of GA in a mouse model of spontaneous systemic lupus
erythematosus,
Lalive and colleagues (p. 1313) find no benefits.
GA might therefore only work in specific diseases.
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BCG inhibits Th2 responses
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Interactions between thymic stromal lymphopoietin (TSLP) and
dendritic cells (DCs) appear crucial for evoking allergic Th2
responses. Bacillus Calmette–Guérin (BCG) strongly
induces T
h1 responses, and
Amakawa and colleagues (p. 1321) show that BCG can convert TSLP-activated DCs from inducing inflammatory
T
h2 cells to inducing regulatory T
h1 cells. The authors speculate
that BCG might be helpful for treating allergy.
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T cell clones mediate both arthritis and pneumonitis
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Rheumatoid arthritis (RA) is often accompanied by extra-articular
manifestations, including interstitial lung disease.
Sakaguchi and colleagues (p. 1331) isolated T cell clones from joints
of SKG-strain mice (which model RA). The clones initiate arthritis
and pneumonitis in nude mice but disease progression appears
relatively T-cell-independent. The authors discuss this, and
the susceptibility of certain tissues to immunopathology in
RA.
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NK cells help mediate skin allograft rejection
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Kawai and colleagues (p. 1343) demonstrate that SCID mice reject
donor allografts lacking MHC class II. CD4
+ T cells and NK cells
infiltrate the grafts and NKG2D ligands are upregulated. Depletion
of NK cells or blocking NKG2D prolongs graft survival. A mechanism
whereby CD4
+ cells recognise allo-peptides, upregulate NKG2D
ligands and thus activate NK cells is proposed.
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Tissue damage may trigger elimination of tissue-specific B cells
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Pemphigus vulgaris (PV) is caused by IgG antibodies to desmoglein
3 (Dsg3).
Amagai and colleagues (p. 1351) show, using a mouse
model of PV, that non-pathogenic B cells producing IgM anti-Dsg3
are eliminated from the periphery if pathogenic IgG anti-Dsg3
monoclonal antibodies are injected. The authors infer that self-reactive
B cells may be ignored until a harmful event occurs.
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Connotea 
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Complement peptide inhibits mast...
Different TCR-CD3 structures on...