Vaccines have been used for over 200 years and are the most effective way of preventing the morbidity and mortality associated with infections. Like other drugs, vaccines can cause adverse events, but unlike conventional medicines, which are prescribed to people who are ill, vaccines are administered to healthy individuals, thus increasing the concern over adverse reactions. Most side effects attributed to vaccines are mild, acute and transient; however, rare reactions such as hypersensitivity, induction of infection, and autoimmunity do occur and can be severe and even fatal. The rarity and subacute presentation of post-vaccination autoimmune phenomena means that ascertaining causality between these events can be difficult. Moreover, the latency period between vaccination and autoimmunity ranges from days to years. In this article, on the basis of published evidence and our own experience, we discuss the various aspects of the causal and temporal interactions between vaccines and autoimmune phenomena, as well as the possible mechanisms by which different components of vaccines might induce autoimmunity.

Common clinical characteristics were observed among 93 patients diagnosed with immune-mediated conditions post-HBVv, suggesting a common denominator in these diseases. In addition, risk factors such as history of autoimmune diseases and the appearance of adverse event(s) during immunization may serve to predict the risk of post-immunization diseases. The ASIA criteria were found to be very useful among adults with post-vaccination events. The application of the ASIA criteria to pediatric populations requires further study.

The objective of this article is to identify common and atypical features of systemic lupus erythematosus diagnosed following hepatitis B vaccination. We analyzed retrospectively the medical records of 10 systemic lupus erythematosus patients from different centers, who developed the disease following hepatitis B vaccination and determined the prevalence of different manifestations and the time association to vaccination. In this case series, 80% of the patients were female, mean age 35 +/- 9 years, of which 20% received one inoculation, 20% received two doses and 60% received all three inoculations. The mean latency period from the first hepatitis B virus immunization and onset of autoimmune symptoms was 56.3 days. All patients were diagnosed with systemic lupus erythematosus, according to the American College of Rheumatology revised criteria within 1 year. The prevalence of some systemic lupus erythematosus manifestations was typical and included involvement of the joints (100%), skin (80%), muscles (60%) and photosensitivity (30%). Other symptoms differed in this unique group of systemic lupus erythematosus patients such as low rate of kidney and hematologic involvement, and a relatively high rate of hepatitis (20%). Neurological (80%) and pulmonary (70%) symptoms were also common in this group. Data from this case-series, and previously documented cases in the literature could only show a temporal relation between hepatitis B vaccination and the appearance of systemic lupus erythematosus. Systemic lupus erythematosus related to vaccine may differ from idiopathic systemic lupus erythematosus in its clinical presentation and may resemble drug-induced systemic lupus erythematosus. Thus, physicians should be alerted to this potential association, its possible long latency period and unique presentations, and be encouraged to report and analyze these cases.

Postpericardial injury syndrome (PPIS) is defined as pericarditis or pericardial effusion that results from recent or earlier injury of the pericardium. The clinical features of this syndrome include fever, leukocytosis, and elevated erythrocyte sedimentation rate. Recent studies have established a connection between this clinical presentation and an underlying autoimmune process. The role of the humoral immune response is well established regarding the pathogenesis of PPIS with elevated titers of different antibodies and immune complexes in the circulation correlating with disease activity. Nevertheless, cell-mediated response by different subgroups of T lymphocyte has a significant importance with direct infiltration of pericardial tissue and fluids. The diagnosis of PPIS is still challenging. A strong connection between specific serological immunological markers and the disease would be of great value in diagnosis and treatment.

Objective Complement system is activated in patients with trauma. Although complement activation is presumed to contribute to organ damage and constitutional symptoms, little is known about the involved mechanisms. Because complement components may deposit on red blood cells (RBC), we asked whether complement deposits on the surface of RBC in trauma and whether such deposition alters RBC function. Design A prospective experimental study Setting Research laboratory Subjects Blood samples collected from 42 trauma patients and 21 healthy donors Intervention None Measurements and Main Results RBC and sera were collected from trauma patients and control donors. RBC from trauma patients (n=40) were found to display significantly higher amounts of C4d on their surface by flow cytometry compared to normal RBC (n=17) (P<0.01). Increased amounts of iC3b were found in trauma sera (n=27) (vs. 12 controls, P<0.01) by ELISA. Incubation of RBC from universal donors (O,Rh-) with trauma sera (n=10) promoted C4d deposition on their surface (vs. 6 controls, P<0.05). Complement-decorated RBC (n=6) displayed limited their deformability (vs. 6 controls, P<0.05) in 2-dimensional microchannel arrays. Incubation of RBC with trauma sera (n=10) promoted the phosphorylation of band 3, a cytoskeletal protein important for the function of the RBC membrane (vs. 8 controls, P<0.05), and also accelerated calcium influx (n=9) and enhanced nitric oxide production (n=12) (vs. 4 and 8 controls respectively, P<0.05) in flow cytometry. Conclusions Our study found the presence of extensive complement activation in trauma patients and presents new evidence in support of the hypothesis that complement activation products deposit on the surface of RBC. Such deposition could limit RBC deformability and promote the production of nitric oxide. Our findings suggest that RBC in trauma patients malfunction, which may explain organ damage and constitutional symptoms that is not accounted for otherwise by previously known pathophysiologic mechanisms.

Systemic lupus erythematosus is a multi-systemic autoimmune disease distinguished by the presence of various autoantibodies. Like most autoimmune diseases, systemic lupus erythematosus is believed to be induced by a combination of genetic, immunologic, and environmental factors, mainly infectious agents. Molecular mimicry between an infectious antigen and self-components is implicated as a pivotal mechanism by which autoimmune diseases such as systemic lupus erythematosus are triggered. Here we review the current evidence of molecular mimicry between different infectious agents and systemic lupus erythematosus.

Fibrosis is a pathological process that includes scar formation and overproduction of extracellular matrix by the connective tissue as a response to tissue damage. The fibrotic process involves multiple organs and results in progressive life-threatening diseases. Today, we know more about the molecular mechanism that leads to fibrosis involving different type of cells, cytokines, chemokines, and tissue enzymes. Fibrosis was considered an irreversible process, at least clinically, and is still usually treated by anti-inflammatory and immunosuppressive agents. No proven antifibrotic therapy has shown efficacy in ameliorating the clinical course of fibrotic diseases, but our current understanding led to the development of different drugs with promising results, like: mycophenolate mofetil, interferon, relaxin, and intravenous immunoglobulin. This review will provide a glance to this heavily investigated subject.

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