Utilizing social networks,blogging and YouTube in allergy and immunology practices

Online social networks are used to connect with friends and family members, and increasingly, to stay up-to-date with the latest news and developments in allergy and immunology. As communication is a central part of healthcare delivery, the utilization of such networking channels in allergy and immunology will continue to grow. There are inherent risks to online social networks related to breaches of patient confidentiality, professionalism and privacy. Malpractice and liability risks should also be considered. There is a paucity of information in the literature on how social network interventions affect patient outcomes. The allergy and immunology community should direct future studies towards investigating how the use of social networks and other technology tools and services can improve patient care.     

Expression of toll-like receptors 2, 4 and 9 is increased in gingival tissue from patients with type 2 diabetes and chronic periodontitis

Rojo‐Botello NR, García‐Hernández AL, Moreno‐Fierros L. Expression of toll‐like receptors 2, 4 and 9 is increased in gingival tissue from patients with type 2 diabetes and chronic periodontitis. J Periodont Res 2012; 47: 62–73. © 2011 John Wiley & Sons A/S Background and Objective: Broad evidence indicates that diabetes both increases the risk and hastens the progression of periodontal disease. Likewise, chronic inflammation or infections seem to provoke insulin resistance and thereby contribute to the development of diabetes and its complications. Innate immune responses, which appear to be altered in individuals with diabetes, are usually mediated by the recognition of pathogens through toll‐like receptors (TLRs). The constitutive expression of some TLRs has been reported in healthy human gingival tissue. Interestingly, the expression of TLRs 2 and 4 is increased with the severity of periodontal disease. Considering that the inflammatory reaction is exacerbated in individuals with diabetes and periodontitis, we suspected that the expression of some TLRs might be increased in gingival tissue in these patients. Material and Methods: In this study, we analyzed, by immunofluorescence, the expression of TLRs 2, 3, 4 and 9 in gingival tissues from healthy individuals and from periodontal patients with or without type 2 diabetes. Results: We found that the expression levels of TLRs 2, 3, 4 and 9 were higher in all periodontal patients than in healthy individuals. The expression of some TLRs was increased in subjects with periodontitis and diabetes relative to subjects with periodontitis but without diabetes; this increase in expression was found particularly in TLR2 and TLR9 in the connective tissue and in TLR4 at the epithelial region. Conclusion: These data suggest that the expression of these TLRs 2, 3, 4 and 9 in gingival tissue is higher in individuals with diabetes because its inflammatory reaction is exacerbated. Additionally, the expression of these TLRS is positively regulated with the severity of periodontal disease.     

Immunoglobulin G4–related sclerosing disease Mimicking sjogren's syndrome: A case report

Immunoglobulin G4–related sclerosing disease (IgG4‐RSD) is a fibroinflammatory condition that has the potential to affect nearly every organ system. Classic histological findings include storiform fibrosis and lymphoplasmacytic infiltrates of immunoglobulin G4 (IgG4)–positive plasma cells. The clinical features of IgG4‐RSD may be an under‐recognized disease process that can mimic other autoimmune disorders, including Sjogren's syndrome. We describe a rare case of IgG4‐RSD involving the salivary glands, initially misdiagnosed as Sjogren's syndrome. Clinical features of IgG4‐RSD can mimic those of other autoimmune disorders affecting the head and neck. Therefore, otolaryngologists should have IgG4‐RSD on their differential when evaluating patients with diffuse salivary gland swelling. Laryngoscope, 126:2242–2245, 2016     

Hypoxia-Inducible Factor-2α Limits Natural Killer T Cell Cytotoxicity in Renal Ischemia/Reperfusion Injury

Natural killer T (NKT) cells are the major early-acting immune cell type and fundamental immune modulators in ischemia-reperfusion injury (IRI). Because lymphocytes are exposed to various oxygen tensions under pathophysiologic conditions, we hypothesize that hypoxia-inducible factors (HIFs) have roles in NKT cell activation, and thus determine the final outcome of renal IRI. In this study, we used Lck-Cre transgenic mice to specifically disrupt HIF-2α in T/NKT cells and found that HIF-2α knockout led to upregulated Fas ligand expression on peripheral NKT cells, but not on conventional T cells. HIF-2α knockout promoted infiltration of NKT cells into ischemic kidneys and exacerbated IRI, which could be mitigated by in vivo NK1.1⁺ cell depletion or Fas ligand blockade. Compared with wild-type NKT cells, HIF-2α^−/− NKT cells adoptively transferred to Rag1-knockout mice elicited more severe renal injury, and these mice were not protected by {"type":"entrez-protein","attrs":{"text":"CGS21680","term_id":"878113053","term_text":"CGS21680"}}CGS21680, an adenosine A2A receptor agonist. Mechanistically, hypoxia-induced expression of adenosine A2A receptor in NKT cells and {"type":"entrez-protein","attrs":{"text":"CGS21680","term_id":"878113053","term_text":"CGS21680"}}CGS21680-induced cAMP production in thymocytes were HIF-2α-dependent. Hydrogen peroxide-induced Fas ligand expression on thymic wild-type NKT cells was significantly attenuated by {"type":"entrez-protein","attrs":{"text":"CGS21680","term_id":"878113053","term_text":"CGS21680"}}CGS21680 treatment, but this effect was lost in HIF-2α^−/− NKT cells. Finally, {"type":"entrez-protein","attrs":{"text":"CGS21680","term_id":"878113053","term_text":"CGS21680"}}CGS21680 and LPS, an inducer of HIF-2α in endothelium, synergistically reduced renal IRI substantially, but this effect was absent in Mx1-Cre-induced global HIF-2α-knockout mice. Taken together, our results reveal a hypoxia/HIF-2α/adenosine A2A receptor axis that restricts NKT cell activation when confronted with oxidative stress and thus protects against renal IRI.     

Ly6Chigh Monocytes Protect against Kidney Damage during Sepsis via a CX3CR1-Dependent Adhesion Mechanism

Monocytes have a crucial role in both proinflammatory and anti-inflammatory phenomena occurring during sepsis. Monocyte recruitment and activation are orchestrated by the chemokine receptors CX3CR1 and CCR2 and their cognate ligands. However, little is known about the roles of these cells and chemokines during the acute phase of inflammation in sepsis. Using intravital microscopy in a murine model of polymicrobial sepsis, we showed that inflammatory Ly6C^high monocytes infiltrated kidneys, exhibited altered motility, and adhered strongly to the renal vascular wall in a chemokine receptor CX3CR1-dependent manner. Adoptive transfer of Cx3cr1-proficient monocyte-enriched bone marrow cells into septic Cx3cr1-depleted mice prevented kidney damage and promoted mouse survival. Modulation of CX3CR1 activation in septic mice controlled monocyte adhesion, regulated proinflammatory and anti-inflammatory cytokine expression, and was associated with the extent of kidney lesions such that the number of lesions decreased when CX3CR1 activity increased. Consistent with these results, the pro-adhesive I249 CX3CR1 allele in humans was associated with a lower incidence of AKI in patients with sepsis. These data show that inflammatory monocytes have a protective effect during sepsis via a CX3CR1-dependent adhesion mechanism. This receptor might be a new therapeutic target for kidney injury during sepsis.     

Activities of erythropoietin on tumors: an immunological perspective

There is a growing interest in the non-erythropoietic, tissue-protective and restorative actions of erythropoietin (EPO). While studies in this field have indicated that EPO can ameliorate chemotherapy-induced peripheral neuropathy and cardiotoxicity, the issue whether EPO can positively or negatively affect cancer patients is a hot one. In this debate, many activities of EPO are being considered, including tissue/neuroprotection, angiogenesis, anti-inflammatory activity, growth promotion, and inhibition of apoptosis. However, few studies have explored the interactions of EPO with the immune system. A study in this issue of the European Journal of Immunology by Katz et al. adds one new piece to the puzzle by showing that EPO can stimulate B cell-mediated immunity.     

CD4+ CD25high regulatory T cells reduce T cell transendothelial migration in cancer patients

Cell-mediated immunity is thought to be the main mechanism of anti-tumour responses of the host, but it is not known if cancer disease affects T cell recruitment from blood to tissues. Therefore, we compared Heliobacter pylori-induced T cell transendothelial migration (TEM) in H. pylori-infected gastric carcinoma patients, colon and lung carcinoma patients and healthy volunteers. H. pylori induced significant T cell migration from all groups. However, there was a dramatic reduction of T cell TEM in gastric carcinoma patients (80%) compared to healthy individuals. A similarly reduced transmigration was also seen in colon and lung carcinoma patients. We found significantly increased frequencies of T(reg) cells in the blood of gastric carcinoma patients compared to healthy individuals, and depletion of T(reg) cells from the blood of these patients prior to TEM restored T cell migration. The effect of T(reg) cells was largely dependent on cell-cell contact, but not on IL-10 or TGF-beta. In addition, the presence of T(reg) cells led to reduced T cell attachment to endothelium and decreased production of T cell-recruiting chemokines during TEM. In conclusion, T(reg) cell-mediated reduction of T cell TEM may reduce T cell recruitment in patients with epithelial malignancies, thereby hampering anti-tumour responses.     

Gaps in Serologic Immunity against Contemporary Swine-Origin Influenza A Viruses among Healthy Individuals in the United States

Influenza A Viruses (IAV) in domestic swine (IAV-S) are associated with sporadic zoonotic transmission at the human–animal interface. Previous pandemic IAVs originated from animals, which emphasizes the importance of characterizing human immunity against the increasingly diverse IAV-S. We analyzed serum samples from healthy human donors (n = 153) using hemagglutination-inhibition (HAI) assay to assess existing serologic protection against a panel of contemporary IAV-S isolated from swine in the United States (n = 11). Age-specific seroprotection rates (SPR), which are the proportion of individuals with HAI ≥ 1:40, corresponded with lower or moderate pandemic risk classifications for the multiple IAV-S examined (one H1-δ1, one H1-δ2, three H3-IVA, one H3-IVB, one H3-IVF). Individuals born between 2004 and 2013 had SPRs of 0% for the five classified H3 subtype IAV-S, indicating youth may be particularly predisposed to infection with these viruses. Expansion of existing immunologic gaps over time could increase likelihood of future IAV-S spillover to humans and facilitate subsequent sustained human-to-human transmission resulting in disease outbreaks with pandemic potential.