RESUMEN
A 25-year-old Caucasian female patient presented with fever and cervical lymphadenopathy. Laboratory findings showed elevated signs of inflammation, elevated ANA titer and strongly positive anti-dsDNA antibodies. The histopathology of the lymph nodes revealed distinct features of Kikuchi-Fujimoto disease, a benign, self-limiting lymphadenopathy that typically affects young Asian females. In the literature a coincidental occurrence of Kikuchi-Fujimoto disease and systemic lupus erythematosus (SLE) is well documented. We hypothesized a simultaneous occurrence of both diseases because of the typical antibodies and arthralgia.
Asunto(s)
Linfadenitis Necrotizante Histiocítica/sangre , Linfadenitis Necrotizante Histiocítica/diagnóstico , Lupus Eritematoso Sistémico/sangre , Lupus Eritematoso Sistémico/diagnóstico , Adulto , Diagnóstico Diferencial , Femenino , HumanosRESUMEN
The influence of the intracellular parasite Toxoplasma gondii on macrophage expression of co-stimulatory molecules was studied. Unlike surface expression of CD80/B7-1, that of CD86/B7-2 is increased in mouse peritoneal macrophages 24 h following exposure to live toxoplasma in vitro. Most CD86 molecules are found on infected cells bearing a maximum parasite load. Consistent with the elevated membrane expression, the quantity of CD86 gene transcript is increased in macrophages infected by T. gondii in vitro or in vivo. CD86 up-regulation contributes to the augmented capacity of parasitized macrophages to present antigen to tuberculin-specific CD4+ T cells as demonstrated by blocking CD86 ligand interaction. T. gondii triggers up-regulation of CD86 in macrophages from BALB/c mice which are resistant to the development of toxoplasmic encephalitis. Infection of macrophages from the susceptible strain BALB.B, however, results in a decreased surface expression of CD86, although the parasite load and intracellular proliferation proved comparable in both macrophages. This differential host cell reaction correlates with disparate profiles in T. gondii-induced cytokine secretion. Upon challenge with toxoplasma, IL-1alpha and tumor necrosis factor (TNF)-alpha are released to a significantly higher extent by BALB/c than by BALB.B macrophages, whereas the latter secrete more IL-12 and IL-10. In BALB.B macrophages, T. gondii-induced IL-10 down-regulates surface expression of CD86, thus indicating an interference of parasite-dependent cytokine release and modulation of CD86. The biased secretory response in macrophages from the two congenic strains implies an MHC-dependent and dichotomous monokine induction by T. gondii. Up-regulation of CD86 seems to occur along the IL-1/TNF-inducing pathway and experimental evidence indicates that this enhances T cell activation by parasitized macrophages.
Asunto(s)
Antígenos CD/biosíntesis , Citocinas/metabolismo , Macrófagos Peritoneales/inmunología , Glicoproteínas de Membrana/biosíntesis , Toxoplasma/inmunología , Toxoplasmosis Animal/inmunología , Animales , Células Presentadoras de Antígenos/inmunología , Antígeno B7-2 , Susceptibilidad a Enfermedades , Antígenos H-2/genética , Inmunidad Innata , Interleucinas/metabolismo , Activación de Linfocitos , Activación de Macrófagos/inmunología , Macrófagos Peritoneales/parasitología , Ratones , Ratones Congénicos , Ratones Endogámicos BALB C/genética , Modelos Inmunológicos , Especificidad de la Especie , Factor de Necrosis Tumoral alfa/metabolismo , Regulación hacia ArribaRESUMEN
According to the economical principle to obtain the highest advantage with the minimalst engagement for the society we passed over in geriatrics from the individual physiotherapy to the therapy in the group, which was very successful in our institution. Four important groups of diseases of the second part of the life have been taken into consideration: Patients with chronic bronchitis, with movement-diseases of the shoulder, the sameone of the hips and the knees and with arterial obturative disease of the extremities.