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Systemic lupus erythematosus (SLE) is a complex, inflammatory autoimmune disease that affects multiple organ systems. We used global gene expression profiling of peripheral blood mononuclear cells to identify distinct patterns of gene expression that distinguish most SLE patients from healthy controls. Strikingly, about half of the patients studied showed dysregulated expression of genes in the IFN pathway. Furthermore, this IFN gene expression \"signature\" served as a marker for more severe disease involving the kidneys, hematopoetic cells, and/or the central nervous system. These results provide insights into the genetic pathways underlying SLE, and identify a subgroup of patients who may benefit from therapies targeting the IFN pathway.

Nasal cutaneous tuberculosis (TB) is a rare manifestation of extrapulmonary tuberculosis and presents a diagnostic challenge, particularly in its paucibacillary form. As demonstrated in this case, achieving laboratory-confirmed diagnosis in paucibacillary TB remains a significant challenge, often resulting in missed or delayed diagnoses and increased severity of disease on presentation. We report an atypical case involving a 19-year-old male with extensive nasal destruction progressing for fourteen years. In this case, lupus vulgaris was ultimately diagnosed after extending the tissue culture duration beyond 35 days, despite prior exclusion of TB as the cause. The patient completed antituberculosis therapy with resolution of the active disease, and he was referred for further management of his facial deformity. The delayed diagnosis led to significant tissue destruction, which could have been prevented with earlier confirmation and treatment of the infection. We propose that, in diagnostically difficult cases, the investigating team consider extending the specimen culture time to the maximum before definitively excluding tuberculous disease.

Antibodies against citrullinated proteins are specific and predictive markers for rheumatoid arthritis although the pathologic relevance of these antibodies remains unclear. To investigate the significance of these autoantibodies, collagen-induced arthritis (CIA) in mice was used to establish an animal model of antibody reactivity to citrullinated proteins. DBA/1J mice were immunized with bovine type II collagen (CII) at days 0 and 21, and serum was collected every 7 days for analysis. Antibodies against both CII and cyclic citrullinated peptide, one such citrullinated antigen, appeared early after immunization, before joint swelling was observed. Further, these antibodies demonstrated specific binding to citrullinated filaggrin in rat esophagus by indirect immunofluorescence and citrullinated fibrinogen by Western blot. To evaluate the role of immune responses to citrullinated proteins in CIA, mice were tolerized with a citrulline-containing peptide, followed by antigen challenge with CII. Tolerized mice demonstrated significantly reduced disease severity and incidence compared with controls. We also identified novel murine monoclonal antibodies specific to citrullinated fibrinogen that enhanced arthritis when coadministered with a submaximal dose of anti-CII antibodies and bound targets within the inflamed synovium of mice with CIA. These results demonstrate that antibodies against citrullinated proteins are centrally involved in the pathogenesis of autoimmune arthritis.

Antecedents. This report presents three cases of Cutaneous tuberculosis CTB that were diagnosed at Calderon Hospital, Quito, Ecuador. The first case was Tuberculosis verrucosa cutis (TVC) in a 44-year-old man with circinated erythematous areas with ulcerated nodules and verruciform plaques from the right lower limb to the hip. The second case was Lupus Vulgaris (LV) in a 50- year-old female with one-year history of pruritic dermatosis in the left ciliary area. The third case was Scrofuloderma in a 23-year-old man with erythematous nodules that drain caseous material at neck, thorax and axillary region. Almost all laboratory tests that were available turned out to have limitations as a diagnostic tool. Conclusion. In immunocompromised and high-risk individuals with atypical lesions, it is important to correlate clinical and epidemiological characteristics with the pretest probability in order to optimize indicators and determine or exclude out the diagnosis.

Lupus vulgaris is a common form of cutaneous tuberculosis in China, mostly involving the head and neck region. Turkey ear is a clinically descriptive term, used for a massively enlarged earlobe with bluish-red or violaceous indurated plaques and nodules, which can be a sign of lupus vulgaris. A 47-year-old female presented with edema and reddish ulcerated lesions on both ears which was diagnosed as lupus vulgaris by conventional laboratory investigations and the patient showed good response to antituberculous therapy. Occurrence of turkey ears in lupus pernio (sarcoidosis) should also be mentioned here as this presentation was originally described in this condition. Two case reports of turkey ear have been reported with cutaneous tuberculosis (not bilateral). However, occurrence of bilateral turkey ears in cutaneous tuberculosis has not been described so far in the literature.

Cutaneous forms of tuberculosis (TB) are rare, comprising about 1-1.5% of all cases, and show a wide range of clinical manifestations. Here we present a case of a patient with left cervical ulcerated lymphadenopathy associated with a violaceous plaque in the area of the manubrium of sternum. We performed a biopsy of the plaque for histopathology, a polymerase chain reaction (PCR) to test for mycobacteria and a smear of the ulcerated lymph node. Histopathology results showed a dermal infiltrate consisting of epithelioid granulomas without necrosis, PCR was negative and the culture was positive for M. tuberculosis. We made the diagnosis of scrofuloderma associated with lupus vulgaris. The patient was treated with an anti-tuberculous therapy with clinical regression of the lesions. Our case emphasizes the importance of recognizing that tuberculosis can occur as a primary cutaneous pathology, with a challenging diagnosis that requires the correlation of clinical findings with diagnostic testing.

In vivo treatment of mice with the natural killer T (NKT) cell ligand, alpha-galactosylceramide (alphaGalCer), ameliorates autoimmune diabetes and experimental autoimmune encephalomyelitis (EAE) by shifting pathogenic Th1-type immune responses to nonpathogenic Th2-type responses. In the current study, in vivo activation of NKT cells in adult NZB/W mice by multiple injections of alphaGalCer induced an abnormal Th1-type immune response as compared with the Th2-type response observed in nonautoimmune C57BL/6 mice. This resulted in decreased serum levels of IgE, increased levels of IgG2a and IgG2a anti-double-stranded DNA (anti-dsDNA) Ab's, and exacerbated lupus. Conversely, treatment of NZB/W mice with blocking anti-CD1d mAb augmented Th2-type responses, increased serum levels of IgE, decreased levels of IgG2a and IgG2a anti-dsDNA Ab's, and ameliorated lupus. While total CD4+ T cells markedly augmented in vitro IgM anti-dsDNA Ab secretion by splenic B cells, the non-CD1d-reactive (CD1d-alphaGalCer tetramer-negative) CD4+ T cells (accounting for 95% of all CD4+ T cells) failed to augment Ab secretion. The CD1d-reactive tetramer-positive CD4+ T cells augmented anti-dsDNA Ab secretion about tenfold. In conclusion, activation of NKT cells augments Th1-type immune responses and autoantibody secretion that contribute to lupus development in adult NZB/W mice, and anti-CD1d mAb might be useful for treating lupus.