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Background Vaccination is a promising strategy to protect vulnerable groups like immunocompromised inflammatory bowel disease [IBD] patients from an infection with SARS-CoV-2. These patients may have lower immune responses. Little is known about the cellular and humoral immune response after a SARS-CoV-2 vaccination in IBD patients. Methods Totals of 28 patients with IBD and 27 age- and sex-matched healthy controls were recruited at Jena University Hospital. Blood samples were taken before, after the first, and in a subgroup of 11 patients after second dose of a SARS-CoV-2 vaccination. Cellular immune response, including IFN-γ and TNF-α response and antibody titres, were analysed. Results Overall, 71.4% of the IBD patients and 85.2% of the controls showed levels of anti-SARS-CoV-2 antibodies above the cutoff of 33.8 BAU/ml [p = 0.329] after the first dose. Even in the absence of SARS-CoV-2 antibodies, IBD patients showed significant T cell responses after first SARS-CoV-2 vaccination compared with healthy controls, which was not influenced by different immunosuppressive regimens. Associated with the vaccination, we could also detect a slight increase of the TNF production among SARS-CoV-2-reactive TH cells in healthy donorsn [HD] and IBD patients. After the second dose of vaccination, in IBD patients a further increase of humoral immune response in all but one patient was observed. Conclusions Already after the first dose of a SARS-CoV-2 vaccination, cellular immune response in IBD patients is comparable to controls, indicating a similar efficacy. However, close monitoring of long-term immunity in these patients should be considered.

Hintergrund Regulatorische T-Zellen (Treg) sind essenziell fur die Aufrechterhaltung der immunologischen Selbsttoleranz, indem sie die Aktivierung und Expansion autoreaktiver Zellen kontrollieren. Sie tragen daher entscheidend zur Verhinderung und Kontrolle von Autoimmunerkrankungen bei.

Objectives Pressure ulcers impose a major lifetime medical problem to patients with high-grade spinal cord injury (SCI). For patients with stages 3-4 pressure ulcers, plastic surgery is often the only remaining treatment option. Despite considerable flap failure rates of around 30%, only sparse knowledge exists on predictors for flap failure. Hence, identification of predictors for flap failures is needed. Methods We prospectively enrolled 38 SCI patients with stages 3-4 pressure ulcers scheduled for plastic surgery. Preoperative wound swabs, intraoperative tissue samples and postoperative drainage liquids were microbiologically analyzed. In multivariable logistic regression analyses, bacterial loads of deep tissue cultures of intraoperative samples as well as other clinical variables were analyzed with respect to the prediction of flap failures. Results The flap failure rate was 27.5%. Bacterial loads of deep tissue cultures were not predictive for flap failure, neither was the colonization with a specific bacterial strain. We observed a considerable fluctuation of microbiological environment from initial swab cultures, intraoperative samples and postoperative drainage fluids. Antibioprophylaxis was sufficient in only 75% of deep tissue cultures and 69% of drainage fluids. Insufficient antibioprophylaxis was associated with a higher flap failure rates (odds ratio 6.3, confidence interval 1.2-41.0). Conclusion After inpatient wound conditioning, bacterial load analysis of intraoperative wound tissue cultures is ineffective in order to predict flap failure rates in SCI patients with stages 3-4 pressure ulcers after flap surgery. Instead, insufficient antibioprophylaxis might be a factor contributing to flap failure.

Das BMBF-geforderte Konsortium IMPAM untersucht in 10 Projekten, koordiniert vom DRFZ Berlin und dem Universitatsklinikum Jena, den molekularen Dialog zwischen immunologischen Gedachtniszellen und mesenchymalen Zellen bei chronisch entzundlichen Gelenkerkrankungen wie der rheumatoiden Arthritis und der ankylosierenden Spondylitis. Ziel ist es, so therapeutisch in diese Interaktionen einzugreifen, dass das pathogene Imprinting der proinflammatorischen Gedachtniszellen geloscht und gleichzeitig die antiinflammatorische Kapazitat korpereigener regulatorischer Zellen bei den Patienten wiederhergestellt wird.

Background and purpose Pressure sores are a major health problem in spinal cord injury (SCI). In this population pressure damage to peripheral nerves was not thoroughly investigated so far. However, intact peripheral nerves and innervated muscles are a prerequisite for the effectiveness of supportive therapies like functional electrical stimulation (FES). Methods We assessed electroneurographic (ENG) data of lower limbs in SCI individuals admitted to our hospital due to severe pressure sores. Our centers prospectively acquired ENG data of the European Multicenter study about SCI (EMSCI) patients served as early control. Results In the pressure sore cohort (n = 15) all patients were sensory-motor complete (American Spinal Cord Injury Association Impairment Scale A). Most patients (10/15) suffered from a severe axonal sensory-motor polyneuropathy in paralysed legs with absent compound muscle action potentials (CMAPs) of tibial/peroneal nerves as well as absent sensory nerve action potentials of sural nerves. The onset of this polyneuropathy dates within the first year after incident SCI and was mainly associated with increasing sensory-motor completeness as demonstrated by a significant CMAP drop of our centers EMSCI-ENG data on serial tibial nerve recordings in 275 patients. Conclusions Severe SCI is associated with an early-onset axonal polyneuropathy in paralysed limbs to which pressure damage might contribute. Because intact peripheral nerves are required for: (i) maintenance of motor function in centrally impaired muscles; and (ii) effectiveness of supportive therapies like FES, ENG-monitoring could serve as a low invasive screening method for peripheral nerve integrity in patients with SCI to initiate pressure relief procedures early enough.

The host response to Borrelia burgdorferi is likely to play a role in the pathogenesis of Lyme arthritis. Whereas most patients with Lyme arthritis can be cured with antibiotic therapy, approximately 10% of the patients have persistent arthritis for months or even several years after antibiotic treatment. In this study, we tested the hypothesis that the T cell response to one or more antigens of B. burgdorferi is different in patients with treatment-responsive or treatment-resistant Lyme arthritis. For this purpose, 313 B. burgdorferi-specific T cell lines were derived from the synovial fluid or peripheral blood of four patients with treatment-responsive Lyme arthritis and five patients with treatment-resistant arthritis. 87 T cell lines from treatment-responsive Lyme arthritis and 112 lines from the treatment-resistant group were examined for the recognition of five recombinant. B. burgdorferi proteins: outer surface proteins A (OspA), B, C, p39, and p93. In both groups of patients, the T cell lines frequently recognized OspB, and only occasionally recognized OspC, p39, and p93. In contrast, OspA was preferentially recognized by T cell lines from patients with treatment-resistant arthritis, but only rarely recognized by T cell lines from patients with treatment-responsive arthritis (odds ratio 28.4, 95% confidence interval 9.2-87.8, p < 0.005). These results are compatible with the hypothesis that the T cell response to B. burgdorferi OspA is involved in the pathogenesis of treatment-resistant Lyme arthritis.

Rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) are chronic inflammatory diseases that primarily affect the joints. The triggers that activate autoreactive T and B lymphocytes in arthritic patients are still unknown.1 It has been widely assumed, however, that the autoantigens recognised by arthritogenic lymphocytes are joint-specific. This assumption has been challenged by findings from a murine model of …

T helper (Th) cells are grouped into functionally different subsets (considered hitherto distinct and stable) according to their cytokine production. However, a number of recent findings show a much higher degree of Th cell plasticity and interconvertibility than previously assumed. Therefore, Th effector functions might be subject to therapeutic modulation even in late stages of immunopathological diseases.

Reactive arthritis (ReA) and Lyme arthritis together comprise a pair of chronic inflammatory diseases of the joints. Although differing in detail, these relatively rare diseases are related in their immunopathology to the much commoner rheumatoid arthritis (RA), for which they serve as both model and control. The trigger for rheumatoid arthritis is unknown, but for these rarer diseases triggering occurs by certain well-defined bacterial infections. Arthritis is an uncommon outcome of these infections, for reasons unknown, and the development of chronic, as distinct from brief, arthritis is even rarer; again, the reasons are unknown. Not only does knowing the trigger greatly assist us in understanding these diseases, so also does knowing the contrasting pattern of Th1 versus Th2 cytokines observed in RA and ReA. ReA and Lyme arthritis are here considered in the wider setting of infections where chronic morbidity arises first from hypersensitivity, and perhaps finally from autoimmunity, such as occurs in some of the major tropical diseases. The immunology of ReA and Lyme disease is surveyed in detail, concentrating on T cells and including an update on the Lyme vaccine(s). Additional sections deal with the enigma of HLA B27, with epidemiological findings relevant to the chronicity of ReA and to the need for enlarged prospective studies of ReA in the setting of a developing country.

Of 686 hemophiliacs who are being treated at our institution, 402 (59%) are HIV-sero-positive. One hundred seventy-eight heterosexual partners of HIV-infected hemophiliacs have been serologically examined; 19 (11%) are HIV-positive. So far none of the seropositive partners suffers from ARC or AIDS. The rate of heterosexual transmission of HIV is statistically significantly correlated with the CD4+ count of the HIV-infected index patient. No such correlation was found with the index patient's clinical stage or the isolation of HIV from the index patient's blood. Of 39 seronegative female partners who were investigated clinically and immunologically, 17 showed pathologically increased numbers of CD8+ counts. In one case, HIV was transmitted from a female patient with von Willebrand's disease to her husband. As compared to other groups at risk for AIDS, the rate of heterosexual HIV transmission is comparatively low in hemophiliacs. The exact reason for this difference is not yet known. The relevance of the immunopathological findings in seronegative sexual partners of hemophiliacs also remains to be determined.

At our institution 686 hemophiliacs are being treated. Of them 402 (59%) are anti-HIV-seropositive. The general use of heat-treated clotting factor products was begun in July 1983, and from May 1984 all patients exclusively used heat-treated clotting factors. Thus, one can assume that infection occurred no later than early 1984 in our patients. Since December 1985 HIV-positive hemophiliacs have regularly been clinically and immunologically examined. Most of the 306 patients who could be investigated were clinically symptom-free at the time of their first visit. However, 45 patients have developed AIDS from 1982 through August 1988. The mean survival time of hemophiliacs with AIDS is less than 6 months. In 36% of those 274 patients who have been followed for a mean period of 14 months the clinical stage of the disease worsened by at least one stage according to the classification system proposed by the Centers for Disease Control. We did not find a correlation between clotting-factor consumption during the years 1984–1986 and the actual clinical stage of the patients. Virus isolation from peripheral blood lymphocytes (PBIs) answered the question whether anti-HIV seropositive hemophiliacs are not only immunized but really infected in many more cases than those revealed by detection of p24 antigen or decline of p24 antibody. Positive viral culture correlated strongly with a drop in CD4+ lymphocytes under the level of 400/µl. However, HIV could not be cultured regularly in advanced cases, suggesting that virus replication in PBLs is not necessarely the cause of depletion of T-helper cells. There is no evidence that the natural history of HIV infection in hemophiliacs is different from that in other HIV-infected patients.

780 hemophiliacs are treated at the Institut fiir experimentelle Hamatologie, University of Bonn. Of these, 61% (475 patients) are infected with HIV.From 1982 through January 1987, 15 of the HIV-infected hemophiliacs developed AIDS. It seems alarming, that 9 patients had theirprimary manifestations of AIDS in 1986 and one in January 1987. The primary manifestations of AIDS were:We describe here the clinical features of the hemophilic AIDS patients and discuss the differences in clinical manifestation and prognosis compared to AIDS-patients belonging to other risk groups.These data are discussed on the background of other clinical, immunological and epidemiological findings in our large cohort of HIV-infected hemophiliacs.