International Immunology 2008 20(6):NP; doi:10.1093/intimm/dxn053
© 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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Immune nephritis in various mouse strains
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The autoantibody formation and the end-organ damage seen in
immune nephritis might be under separate genetic control, so
it is important to characterise murine strains that might model
the human disease. In this issue,
Mohan and colleagues (p. 719) describe the susceptibility of eight strains of inbred mice
to antibody-induced immune nephritis. The characteristics of
disease in each strain are detailed.
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Regulatory B1 cells in colitis
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Bhan and colleagues (p. 729) examined a strain of mice that
are genetically susceptible to chronic colitis and that were
kept for several generations in specific-pathogen-free facilities
compared with conventional facilities; colitis was suppressed
in the latter. The authors show a role for B-1 B cells and natural
IgM production in this protection and discuss potential implications
for the ‘hygiene hypothesis’.
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IL-27 promotes the onset of colitis
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IL-27 is closely related to IL-6, IL-12 and IL-23, which play
an important role in diseases such as inflammatory bowel disease.
Villarino et al. (p. 739) ablated IL-27-specific effects and
thereby reduced pathology in a model in which colitis can be
either spontaneous or triggered by helminth infection. The authors
also investigated the effects on T
h1 and T
h2 responses.
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SOCS-1 ameliorates inflammatory bowel disease
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Proinflammatory cytokines are known to play an important role
in inflammatory bowel disease (IBD). Suppressor of cytokine
signalling 1 (SOCS-1) is an important inhibitor of such cytokines.
In the study by
Naka and colleagues (p. 753), SOCS-1
+/– mice had more-severe colitis than wild-type mice do in a model
of IBD. The authors highlight the role of IFN-
in this process.
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Marginal zone B cells require Delta-like 1
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Notch2 signals triggered by Delta-like 1 (Dll1) are important
for generation of marginal zone B cells (MZB) in spleen, and
MZB are important for autoantibody production.
Moriyama et al. (p. 763) generated a panel of monoclonal antibodies against
Notch receptors and their ligands. MZB development and maintenance
were decreased by blocking Dll1 in normal mice, but MZB maintenance
in lupus-prone mice was Dll1-independent; these results implicate
MZB dysregulation in autoimmunity.
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Osteoclasts support plasma cell survival
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The long-term survival of antibody-secreting plasma cells may
depend on the environmental niche, for example bone marrow or
inflammatory sites. Here,
Pellat-Deceunynck and colleagues (p. 775) show that both osteoclasts and dendritic cells mediate
terminal differentiation of normal plasma cell precursors; however,
osteoclasts are much better at supporting survival of plasma
cells. The authors also investigated the role of cell–cell
contact in this system.
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IL-2 plus anti-IL-2 induces antitumor NK cells
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Previous work has shown that combined administration of IL-2
and anti-IL-2 antibodies protects against tumours better than
either agent alone.
Murakami and colleagues (p. 783) used depletion
studies to show that NK cells, rather than dendritic cells or
CD8
+ cells, mediate this effect. The authors discuss the implications
for therapeutic use of IL-2.
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IL-33 induces type 2 responses without T cell help
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IL-18 and IL-33 are members of the IL-1 superfamily. Significant
differences were found when
Nakanishi and colleagues (p. 791) compared cytokine production by basophils, mast cells and T
h2
cells in response to IL-33 or IL-18.
In vivo, IL-33 can induce
airway hyper-responsiveness and goblet cell hyperplasia in mice
lacking T and B lymphocytes, with clear implications for innate
responses in asthma.
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