Dendritic cells (DCs) 3 are the most potent antigen-presenting cells of the immune system and are specialized to sensitize helper and killer T cells during the induction of T cell-mediated immunity (1, 2). In fact, DCs are the only antigen-presenting cells that are able to stimulate naive CD4 ϩ and CD8 ϩ T cells and are therefore referred to as "nature's adjuvant."The CD83 molecule is to date the best known marker for fully mature DCs because CD83 is predominantly expressed on the surface of dendritic lineage cells and cannot be detected on immature DC precursors (3-5). Although its exact function remains to be determined, the fact that CD83 expression is activated during DC maturation, together with co-stimulatory molecules such as CD80 and CD86, suggests a functionally important role for CD83 in DC-mediated T cell immunity (6, 7). This notion is also supported by the fact that inhibition of CD83 expression during DC maturation reduces the T cell stimulatory capacity of these DCs in allo-mixed leukocyte reactions (8). A study using the soluble extracellular domain of CD83 has provided the first direct evidence that this specific surface molecule is indeed functionally important for T cell activation; the soluble CD83 protein completely inhibited DC-mediated T cell stimulation in a concentration-dependent manner in vitro (9). These data were subsequently confirmed in an independent study by using CD83-Ig fusion protein (10). Thus, CD83 appears to play an important functional role in the regulation of DC-mediated T cell-specific immune responses. Therefore, the investigation of the regulation of CD83 expression may provide novel opportunities to modulate DC activity and subsequently DC-mediated immune responses.

BackgroundGammaherpesviruses (GHVs) are a large group of dsDNA viruses that can infect humans and several animal species. The two human GHVs, Epstein-Barr virus and Kaposi’s sarcoma-associated herpesvirus are known for their oncogenic properties in individuals with immunodeficiency. Recently, the first feline GHV, Felis catus gammaherpesvirus 1 (FcaGHV1) was discovered and frequently found in domestic cats in Australia, Singapore and the USA. FcaGHV1 is more likely to be detected in cats co-infected with the feline immunodeficiency virus (FIV).FindingsThe prevalence of FcaGHV1 in pet cats from Germany and Austria was 16.2 % (95 % CI = 12.38-20.02). The odds for GHV infection were greater for FIV positive (OR = 4.5), male (OR = 13.32) and older (OR = 2.36) cats. Furthermore, FcaGHV1 viral loads were significantly higher in FIV-infected cats compared to matched controls.ConclusionsGHV infections are common in domestic cats in Central Europe. The worldwide distribution of FcaGHV1 can be assumed. A potential role as a co-factor in FIV-induced pathogeneses is supported.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-015-0381-6) contains supplementary material, which is available to authorized users.

In domestic cats, the AB blood group system consists of the three types A, B, and C (usually called AB), which vary in frequency among breeds and geographic regions. Mismatches cause acute hemolytic transfusion reactions and hemolysis of the newborn due to the presence of naturally occurring anti-A alloantibodies. Cytidine monophosphate-N-acetylneuraminic acid hydroxylase (CMAH) converts N-acetylneuraminic acid (type B) to N-glycolylneuraminic acid (type A), and type C erythrocytes express both antigens. We examined the feline CMAH coding regions and genotyped cats to characterize type A, B, and C animals. Of 421 phenotypically typed cats, 60% were A, 35% B and 5% C. Among the 70 cats for which the CMAH coding region was sequenced, 13 new variants were identified in addition to 16 of the previously reported 18 variants. The CMAH variant c.268T>A is seen in type B cats of most breeds, and the variant c.179G>T results in type B in Turkish breeds. The variants c.1322delT and c.933delA cause frameshifts with early stop codons and thereby type B in some Ragdolls and domestic shorthair cats, respectively. Protein modeling with PROVEAN affirmed their deleterious effects. No type A and C cats had more than one allele with one of the above variants. Variant analysis of three SNVs (c.142G>A, c.268T>A and Δ-53) and blood typing of an additional 351 typed cats showed complete phenotype-genotype concordance. In conclusion, the three CMAH variants c.179G>T, c.268T>A and c.1322delT are the main reasons for the defective NeuGc synthesis causing blood type B in domestic purebred and non-pedigreed cats. Together with the variant c.364C>T for type C in Ragdolls they offer a molecular screening scheme for clinical diagnostics to assure blood type compatibility.

No abstract

Hemophilia A is the most common coagulation factor disorder in humans and dogs. The disease is characterized by the lack or diminished activity of Factor VIII (FVIII), caused by variants in the F8 gene and inherited as an X chromosomal trait. Two related male Rhodesian Ridgebacks were diagnosed with Hemophilia A due to reduced FVIII activity. The purpose of the study was to determine the genetic cause and give breeding advice for the remaining family members in order to eradicate the variant. By Sanger sequencing a short interspersed nuclear element (SINE) insertion in exon 14 of the F8 gene was found. Perfect correlation of this genetic variant with clinical signs of hemophilia A in the family tree, and the lack of this genetic variant in more than 500 unrelated dogs of the same and other breeds, confirms the hypothesis of this SINE being the underlying genetic cause of Hemophilia A in this family. The identification of clinically unaffected female carriers allows subsequent exclusion of these animals from breeding, to avoid future production of clinically affected male offspring and more subclinical female carriers.