- ►diabetesjournals.org AP Martin, S Rankin, S Pitchford, IF Charo, GC Furtado, … - Diabetes, 2008 - Am Diabetes Assoc RESEARCH DESIGN AND METHODS—We tested the hypothesis that macrophage accumulation
into the islets is caused by overexpression of the chemokine CCL2. To test this hypothesis, we
generated transgenic mice and evaluated the cellular composition of the islets by ... Cited by 5 - Related articles - All 3 versions
LJ Yang - Diabetes, 2008 - Am Diabetes Assoc Type 1 diabetes is conventionally thought to result from T-cell–mediated autoimmune destruction
of pancreatic β-cells (1–3). Experimental and clinical evidence accumulated over the past two
decades indicates that T-cells play a critical role in the pathogenesis of type 1 diabetes in ... Related articles - All 3 versions
C Gysemans, H Callewaert, F Moore, M Nelson-Holte, … - Diabetologia, 2009 - Springer Abstract Aims/hypothesis IFN-γ, together with other inflammatory cytokines such as IL-1β and
TNF-α, contributes to beta cell death in type 1 diabetes. We analysed the role of the transcription
factor interferon regulatory factor (IRF)-1, a downstream target of IFN-γ/signal transducer ... Related articles - All 2 versions
MJ Richer, MS Horwitz - Journal of Innate Immunity, 2009 - content.karger.com To protect against viral infection, the immune response is critically dependent on innate sensing
mechanisms to provide rapid detection of pathogens and allow for the development of an appropriate
adaptive immune response. Mounting evidence suggests that mechanistic differences in ... Related articles - All 3 versions
DL Eizirik, ML Colli, F Ortis - Nature Reviews Endocrinology, 2009 - phx1.medscape.com Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disease with a strong inflammatory
component. The latest studies indicate that innate immunity and inflammatory mediators have
a much broader role in T1DM than initially assumed. Inflammation might contribute to ... Cited by 8 - Related articles - All 8 versions
EN Gurzov, F Ortis, L Bakiri, EF Wagner, DL Eizirik - PLoS One, 2008 - pubmedcentral.nih.gov Cytokines contribute to pancreatic β-cell apoptosis in type 1 diabetes (T1D) by modulation of
β-cell gene expression networks. The transcription factor Activator Protein-1 (AP-1) is a key regulator
of inflammation and apoptosis. We presently evaluated the function of the AP-1 subunit ... Cited by 8 - Related articles - All 7 versions
J De Miranda, K Yaddanapudi, M Hornig, WI Lipkin - The FASEB Journal, 2009 - FASEB RNA virus replication results in expression of double-stranded RNA (ds-RNA) molecules that
trigger innate immune responses through interactions with both intracellular and extracellular
receptors. We investigated the contributions of the extracellular and intracellular ... Cited by 1 - Related articles - All 4 versions
- ►diabetesjournals.org F Moore, ML Colli, M Cnop, MI Esteve, AK Cardozo, DA … - Diabetes, 2009 - Am Diabetes Assoc OBJECTIVE The pathogenesis of type 1 diabetes has a strong genetic component.
Genome-wide association scans recently identified novel susceptibility genes including the phosphatases
PTPN22 and PTPN2. We hypothesized that PTPN2 plays a direct role in β-cell demise ... Cited by 1 - Related articles - All 3 versions
- ►nih.gov S Zhou, EA Kurt-Jones, AM Cerny, M Chan, RT … - The Journal of …, 2009 - jvi.highwire.org Myeloid differentiation factor 88 (MyD88) is an essential adaptor protein in the Toll-like
receptor-mediated innate signaling pathway, as well as in interleukin-1 receptor (IL-1R) and
IL-18R signaling. The importance of MyD88 in the regulation of innate immunity to ... Cited by 1 - Related articles - All 6 versions
