BackgroundQuite a few randomized controlled trials (RCTs) investigating the efficacy of platelet-rich plasma (PRP) for treatment of knee osteoarthritis (OA) have been recently published. Therefore, an updated systematic review was performed to evaluate the temporal effect of PRP on knee pain and physical function.MethodsPubmed, Embase, Cochrane library, and Scopus were searched for human RCTs comparing the efficacy and/or safety of PRP infiltration with other intra-articular injections. A descriptive summary and quality assessment were performed for all the studies finally included for analysis. For studies reporting outcomes concerning Western Ontario and McMaster Universities Arthritis Index (WOMAC) or adverse events, a random-effects model was used for data synthesis.ResultsFourteen RCTs comprising 1423 participants were included. The control included saline placebo, HA, ozone, and corticosteroids. The follow-up ranged from 12 weeks to 12 months. Risk of bias assessment showed that 4 studies were considered as moderate risk of bias and 10 as high risk of bias. Compared with control, PRP injections significantly reduced WOMAC pain subscores at 3, 6, and 12 months follow-up (p = 0.02, 0.004, <0.001, respectively); PRP significantly improved WOMAC physical function subscores at 3, 6, and 12 months (p = 0.002, 0.01, <0.001, respectively); PRP also significantly improved total WOMAC scores at 3, 6 and 12 months (all p < 0.001); nonetheless, PRP did not significantly increased the risk of post-injection adverse events (RR, 1.40 [95% CI, 0.80 to 2.45], I 2 = 59%, p = 0.24).ConclusionsIntra-articular PRP injections probably are more efficacious in the treatment of knee OA in terms of pain relief and self-reported function improvement at 3, 6 and 12 months follow-up, compared with other injections, including saline placebo, HA, ozone, and corticosteroids.Review registrationPROSPERO CRD42016045410. Registered 8 August 2016.Electronic supplementary materialThe online version of this article (doi:10.1186/s13018-017-0521-3) contains supplementary material, which is available to authorized users.
Programmed death-ligand (PD-L)1 and PD-L2, newer B7 superfamily members, are implicated in the negative regulation of immune responses and peripheral tolerance. To examine their function in alloimmunity, we used the murine model of orthotopic corneal transplantation. We demonstrate that PD-L1, but not PD-L2, is constitutively expressed at high levels by the corneal epithelial cells, and at low levels by corneal CD45+ cells in the stroma, whereas it is undetectable on stromal fibroblasts and corneal endothelial cells. Inflammation induces PD-L1 up-regulation by corneal epithelial cells, and infiltration of significant numbers of PD-L1+CD45+CD11b+ cells. Blockade with anti-PD-L1 mAb dramatically enhances rejection of C57BL/6 corneal allografts by BALB/c recipients. To examine the selective contribution of donor vs host PD-L1 in modulating allorejection, we used PD-L1−/− mice as hosts or donors of combined MHC and minor H-mismatched corneal grafts. BALB/c grafts placed in PD-L1−/− C57BL/6 hosts resulted in pronounced T cell priming in the draining lymph nodes, and universally underwent rapid rejection. Allografts from PD-L1−/− C57BL/6 donors were also significantly more susceptible to rejection than wild-type C57BL/6 grafts placed into BALB/c hosts, primarily as a result of increased T cell infiltration rather than enhanced priming. Taken together, our results identify differential roles for recipient vs donor PD-L1 in regulating induction vs effector of alloimmunity in corneal grafts, the most common form of tissue transplantation, and highlight the importance of peripheral tissue-derived PD-L1 in down-regulating local immune responses.
Immune inhibitory receptor genes that encode a variable (V) region, a unique V-like C2 (V͞C2) domain, a transmembrane region, and a cytoplasmic tail containing immunoreceptor tyrosine-based inhibition motifs (ITIMs) have been described previously in two lineages of bony fish. In the present study, eleven related genes encoding distinct structural forms have been identified in Ictalurus punctatus (channel catfish), a well characterized immunological model system that represents a third independent bony fish lineage. Each of the different genes encodes an N-terminal V region but differs in the number of extracellular Ig domains, number and location of joining (J) region-like motifs, presence of transmembrane regions, presence of charged residues in transmembrane regions, presence of cytoplasmic tails, and͞or distribution of ITIM(s) within the cytoplasmic tails. Variation in the numbers of genomic copies of the different gene types, their patterns of expression, and relative levels of expression in mixed leukocyte cultures (MLC) is reported. V region-containing immune-type genes constitute a far more complex family than recognized originally and include individual members that might function in inhibitory or, potentially activatory manners. E xtended multigene families belonging to the Ig gene superfamily (IgSF) account for a diverse range of immunological functions including recognition of antigens and antigenic peptides by both somatically rearranging Ig and T cell antigen receptor (TCR) genes, as well as by major histocompatibility complex (MHC) molecules. The origins of the three diverse systems of effector molecules can be traced through analyses of these genes in extant species of representative early, jawed vertebrates (1). Recently, multigene families which encode novel immune-type receptors (NITR͞nitr) have been described in Spheroides nephelus (Southern pufferfish; ref. 2) and Danio rerio (zebrafish; ref. 3). The NITR genes described in these species encode two extracellular Ig domains [a variable (V) domain and a V-like C2 (V͞C2) domain], a transmembrane region, and most often, immunoreceptor tyrosine-based inhibition motifs (ITIMs) in the cytoplasmic tail. The general structural characteristics of the NITR V domain are common to the corresponding regions of both Ig and TCR (4); whereas ITIMs are found in several inhibitory receptors, which are encoded at the leukocyte receptor cluster (LRC) on human chromosome 19q13.3-13.4 and at a corresponding location on mouse chromosome 7 and include natural killer (NK) receptors, such as killer cell Ig-type receptors (KIRs) (5). Unlike NITR genes, LRC genes do not encode V regions. A number of questions arise regarding the distribution of the NITR genes in vertebrate phylogeny, their function, and the relatedness of NITR genes to other families of genes that are involved in immune function, specifically, the immune inhibitory receptors of the mammalian LRC.The lack of immunologically relevant in vitro culture systems in pufferfish and zebrafish severely limits fun...
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