Differential Expression of O-Glycans in CD4(+) T Lymphocytes from Patients with Systemic Lupus Erythematosus.

T cells from patients with systemic lupus erythematosus (SLE) show a decreased activation threshold and increased apoptosis. These processes seem to be regulated by glycosylated molecules on the T cell surface. Here, we determined through flow cytometry the expression of mucin-type O-glycans on T helper cells in peripheral blood mononuclear cells (PBMC) from 23 SLE patients and its relation with disease activity. We used lectins specific for the disaccharide Gal-GalNAc, such as Amaranthus leucocarpus lectin (ALL), Artocarpus integrifolia lectin (jacalin) and Arachis hypogaea lectin (peanut agglutinin, PNA), as well as lectins for sialic acid such as Sambucus nigra agglutinin (SNA) and Maakia amurensis agglutinin (MAA). The results showed that ALL, but not jacalin or PNA, identified significant differences in O-glycan expression on T helper cells from active SLE patients (n = 10). Moreover, an inverse correlation was found between the frequency of T helper cells recognized by ALL and SLE Disease Activity Index (SLEDAI) score in SLE patients. In contrast, SNA and MAA lectins did not identify any differences between CD4(+) T cells from SLE patients. There was no difference in the recognition by ALL on activated T helper cells and T regulatory (Treg) cells. Our findings point out that activation of SLE disease diminishes the expression of O-glycans in T helper cells; ALL could be considered as a marker to determine activity of the disease.

Transfer factor and allergy.

Although various mechanisms involving antibodies and various cell types participate, a Thl and Th2 cells imbalance seems to play a central role for allergy development. Other lymphocyte subpopulations, such as Th17, CD4 FOXP3, and Th9 positive regulatory T lymphocytes may also be involved in the allergic response. Regulatory processes are an appealing target for therapeutic approaches aiming to solve allergic reactions by restoring the delicate balance within the immune system. Transfer factor (TF) or dialyzable leukocyte extract is meant to transfer cell-mediated immunity from immune competent donors to unsensitized or deficient recipients. A PubMed search on the current knowledge on TF indicates that TF may restore the Th1/Th2 balance and improve immune regulatory mechanisms of patients receiving it. Our preliminary results demonstrate that TF induces mRNA expression of IFN-g, osteopontin, RANTES, and hBD-2 in human healthy subjects. TF has been used to treat a variety of immune dysfunction related-pathologies, such as allergy, autoimmunity, immunodeficiencies, infectious diseases and tumors. Patients receiving TF together with their conventional treatment often have better clinical evolution than without it, as we have witnessed, adding TF to the usual medical treatment of allergic diseases as an attempt to provide allergic patients with those regulatory elements that they apparently lack but require to achieve properly regulated immune responses and thus obtain a faster and better resolution of allergic reactions.

Indications, usage, and dosage of the transfer factor.

The transfer factor (TF) was described in 1955 by S. Lawrence. In 1992 Kirkpatrick characterized the specific TF at molecular level. The TF is constituted by a group of numerous molecules, of low molecular weight, from 1.0 to 6.0 kDa. The 5 kDa fraction corresponds to the TF specific to antigens. There are a number of publications about the clinical indications of the TF for diverse diseases, in particular those where the cellular immune response is compromised or in those where there is a deficient regulation of the immune response. In this article we present our clinical and basic experiences, especially regarding the indications, usage and dosage of the TF. Our group demonstrated that the TF increases the expression of IFN-gamma and RANTES, while decreases the expression of osteopontine. Using animal models we have worked with M. tuberculosis, and with a model of glioma with good therapeutic results. In the clinical setting we have worked with herpes zoster, herpes simplex type I, herpetic keratitis, atopic dermatitis, osteosarcoma, tuberculosis, asthma, post-herpetic neuritis, anergic coccidioidomycosis, leishmaniasis, toxoplasmosis, mucocutaneous candidiasis, pediatric infections produced by diverse pathogen germs, sinusitis, pharyngitis, and otits media. All of these diseases were studied through protocols which main goals were to study the therapeutic effects of the TF, and to establish in a systematic way diverse dosage schema and time for treatment to guide the prescription of the TF.

Avances en el estudio de los mecanismos celulares de supresión de la respuesta inmunitaria en la tuberculosis / Advances in the study of immunosuppression cell mechanisms in tuberculosis

La respuesta inmunitaria protectora generada durante la tuberculosis es el resultado de la integración de las respuestas inmunitarias, natural y adquirida, a través de la activación de linfocitos T CD4+ productores de IFN-g, permitiendo la eliminación del bacilo por macrófagos activados. La inmunosupresión, es la consecuencia de un desequilibrio en la respuesta inmunitaria con progreso de la infección. En este trabajo, se revisan las características de la respuesta inmunitaria contra Mycobacterium tuberculosis así como los mecanismos celulares de supresión de la respuesta inmunitaria.

Oxido nítrico, una molécula multifuncional / Nitric oxide, a multifunctional molecule

El óxido nítrico es un regulador importante de diversas funciones fisiológicas y además, es un factor que contribuye a la respuesta inmune innata. Su efecto también puede estar relacionado a procesos patológicos como el asma o la inflamación crónica. Objetivo. En este trabajo se revisaron algunos aspectos bioquímicos, inmunológicos y fisiopatológicos del óxido nítrico

Actividad fagocítica de monocitos de sangre venosa de pacientes con tuberculosis pulmonar / Phagocytic activity of venous blood monocytes from patients with pulmonary tuberculosis

El papel que desempeña el macrófago en los individuos infectados con Mycobacterium tuberculosis es fundamental al inicio y durante el curso de la infección. En este trabajo, presentamos la actividad fagocítica in vitro de monocitos de sangre venosa aislados de pacientes tuberculosos. El parámetro estudiado fue la capacidad de los macrófagos para fogocitar eritrocitos de carnero en ensayos in vitro el cual se expresa como índice fagocítico(IF). Los resultados muestran que el IF se encuentra disminuido en los macrófagos de pacientes con tuberculosis PPD- y, en forma más evidente, en los pacientes PPD+ con respecto al IF mostrado por los macrófagos de individuos sanos. Estos resultados sugieren que la disfunción de la fagocitosis en los macrófagos de pacientes con tuberculosis contribuye a la cronicidad de la infección

Moléculas de cooperación y regulación durante la migración celular en la respuesta inflamatoria / Molecules for cooperation and regulation during cell migration in the inflammatory response

En la superficie de todas las células existen estructuras sacarídicas, dentro de sus múltiples funciones fisiológicas se ha logrado identificar que funcionan como comunicadores intercelulares. En el caso de los leucocitos estas estructuras le permiten, por mecanismos de adherencia, identificar a los sitios de inflamación, este proceso se efectúa gracias a la interacción específica de diversas familias de glicoproteínas de superficie celular entre las que se considera a las denominadas "selectinas", las integrinas y las moléculas pertenecientes a la superfamilia de las inmunoglobulinas. En este Trabajo, se revisan las características moleculares de estas proteínas adhesivas y, los diversos procesos inflamatorios en los que están involucradas