¿Es el peso de las mochilas escolares lo que ocasiona dolor de espalda a los niños de 10-11 años de edad? / Does the weight of backpacks cause backache in 10-11 year-old children?

Introducción: El dolor de espalda es una patología cada vez más prevalente, produce un alto absentismo laboral, genera un alto coste tanto sanitario como económico y entraña una alta posibilidad de cronificación que, en muchos casos, se inicia en edades muy tempranas. Se ha relacionado con el uso y el peso de las mochilas que llevan los escolares, y se ha llegado a promover el uso de un determinado peso máximo para evitarlo. Objetivo: Conocer si es el peso de las mochilas escolares lo que realmente ocasiona dolor de espalda a los niños de 10-11años de edad y averiguar cuáles son los factores de riesgo que pueden estar relacionados con este dolor. Métodos: Estudio transversal realizado en 834 niños de 10-11 años de edad mediante entrevista, mediciones personales y cuestionarios; se determinó la talla de los niños y el peso de los niños y las mochilas; se hizo a los niños una serie de preguntas sobre hábitos de vida, antecedentes familiares, presencia y frecuencia de dolor de espalda y factores de posible origen psicosomático; se recogió un segundo cuestionario a los 6 meses del primero, analizando la presencia y la frecuencia de dolor de espalda y los mismos factores de posible origen psicosomático. Resultados: La prevalencia del dolor de espalda fue del 26,6%. Se ha encontrado una relación estadísticamente significativa entre el dolor de espalda y las siguientes variables: a) sexo, con más frecuencia entre las chicas (odds ratio [OR]=1,74; p <0,001); b) dolor de espalda de los progenitores (OR=2,90; p <0,001); c) dolor de espalda de los hermanos mayores (OR= 2,32; p <0,001); d) dolor de cabeza (OR= 2,49; p <0,001);e) dolor abdominal (OR= 2,29; p <0,001), y f) despertares nocturnos (OR= 1,85; p <0,005). La frecuencia del dolor de espalda se correlaciona con la combinación del peso de la mochila y el tiempo que tarda el sujeto en ir y volver andando al colegio (p <0,005). No hemos hallado ninguna relación con las variables talla, peso, pies planos, corrección de pies planos, forma de ir al colegio, forma de sentarse, sedentarismo, toma de medicamentos, tipo de mochila, forma de carga ni peso de la mochila. Conclusiones: Los factores de riesgo identificados en este estudio y relacionados con el dolor de espalda en la población estudiada son el sexo, los antecedentes familiares, otros factores de tipo psicosomático y la combinación del peso de la mochila con el tiempo que se lleva cargando (AU)

Introduction: The backaches are a more daily prevalent pathology, which produces a great absenteeism from work generating a high sanitary and economical cost, and with the possibility of becoming a frequent chronic pathology, that in many cases occurs at early ages. It has been related to the use and weight of the backpacks, which are used, by school children and the promotion of a determined weight to avoid problems are being used. The main goal of this study is to determine whether weight of schoolbags is actually causing backache in children aged 10 and 11, plus evaluating different risk factors that may influence the occurrence of these pains. Methods: A transversal study was conducted with 834 children, aged 10 to 11 years, through interviews and personal measurements through a questionnaire; children where measured and weighed Children were measured, and children and backpacks were weighted; a series of questions were done to them on life habits, familiar precedents, presence and frequency of backache and factors of possible psychosomatic origin; the second questionnaire was gathered 6 months after the first one, analyzing the presence and frequency of backache and the same factors of possible psychosomatic origin. Results: Backache prevalence was of 26.6%. Statistically significant relationships between backache and the following factors were found: a) gender, being this more frequent among females with an OR= 1.74 (p <0.001). b) Parents’ backache: it is more frequent among children having parents who have suffered backache (p <0.001), with an OR= 2.90. c) Older siblings’backache, with an OR= 2.32. d) Headache: (p <0.001), OR= 2.49.e) Abdominal pain: (p <0.001), OR= 2.29. f) Waking up at night: OR= 1.85 (p <0.005). Moreover, backache frequency was correlated to the combination of two factors: the weight of backpacks and the time it takes for the individual to walk back and forth to school (p <0.005). We have found no association between back pains and height, weight, flat feet, flat feet correction, means to get to school, ways of sitting, sedentariness, drug ingestion, types of backpacks, ways of carrying the backpacker the weight of backpacks. Conclusions: We have identified the following risk factors for back pain in school children: gender, family background, other psychosomatic factors and the combination between the weight of backpacks and the time it takes to carry them (AU)

Different proinflammatory cytokine serum pattern in neonate patients undergoing open heart surgery. Relevance of IL-8.

The purpose of this work was to investigate the clinical significance of serum levels of proinflammatory cytokines in pediatric patients undergoing cardiopulmonary bypass. We divided the patients in two groups: 8 neonates, and 19 non-newborn children. IL-1beta, IL-6, IL-8, and TNF serum levels were quantified before sternotomy, at admission to the PICU (30 min postoperatively), 24 h after the onset of surgery and 3 days after the operation. Surgical cardiac stress elicits significant increments of IL-6, IL-8 and TNF serum concentrations in both neonates and non-neonates, regardless of their preoperative clinical condition. However, in newborns the magnitude of the proinflammatory cytokine increments was, in particular with IL-8, remarkably greater than in older children. Moreover, neonate and non-neonate patients showed clearly disparate patterns of serum concentrations over time of both IL-8 and TNF. There was a marked relationship between IL-8 levels and postoperative morbidity, evaluated by pulmonary dysfunction, days on inotropic support and days of PICU stay in both neonates and non-neonates patients. In contrast, we found no relationship between serum levels of IL-6 and TNF and postoperative clinical data. Newborn and non-newborn patients undergoing cardiopulmonary bypass exhibit dissimilar patterns of proinflammatory cytokines. IL-8 might be implicated in the multiorganic dysfunction related to cardiopulmonary bypass in pediatric patients.

Newborn patients exhibit an unusual pattern of interleukin 10 and interferon gamma serum levels in response to cardiac surgery.

OBJECTIVE: The aim of this study was to determine the clinical significance of serum levels of interleukin 10 and interferon gamma in pediatric patients undergoing cardiopulmonary bypass. METHODS: We divided the patients into 2 groups: 8 neonates and 19 non-newborn children. Interleukin 10 and interferon gamma serum levels were quantified before sternotomy, at admission to the pediatric intensive care unit (30 minutes postoperatively), 24 hours after the onset of the operation, and 3 days after the operation. RESULTS: Newborn patients displayed significantly greater amounts of serum interleukin 10 than older children, not only in regard to the peak level achieved but also at every postoperative time point analyzed. In contrast, no significant changes in interferon gamma serum levels were observed in neonates at any time point, whereas non-newborn pediatric patients showed a significant increase in interferon gamma serum concentrations immediately after the operation. This unusual pattern of cytokine response in newborn patients was not associated with modifications in cortisol serum levels. Furthermore, although neonates had significantly different surgical and clinical variables than did the non-newborn pediatric patients, the variation in interleukin 10 production in neonates could not be accounted for by differences in the magnitude of surgical injury. In the group of neonates, there were significant positive correlations between peak interleukin 10 serum levels and both partial pressure of arterial oxygen/fraction of inspired oxygen ratio and postoperative body weight gain. CONCLUSIONS: Newborn patients undergoing cardiopulmonary bypass exhibit a distinctive biologic response pattern characterized by high levels of serum interleukin 10 without changes in serum interferon gamma. This cytokine imbalance could have potential clinical implications.

The internal rotavirus protein VP6 primes for an enhanced neutralizing antibody response.

We studied in the rotavirus system whether the internal protein VP6 could prime for an enhancement in the production of neutralizing antibodies (NeuAb) against the external proteins, VP7 and VP4. It was found that BALB/c mice immunized with recombinant YM VP6 protein, and challenged i.p. with a heterologous rotavirus had an increase in the production of serum NeuAb compared to the control. This response was both homotypic and heterotypic, and involved an increase of NeuAb belonging to the IgM and IgG isotypes. Mice immunized with the recombinant VP6 and challenged orally with infectious murine rotavirus cleared the infection one day earlier than the control not immunized with VP6, and showed a small increase of total fecal anti-rotavirus IgA. The results suggest that the T-helper (Th) cells specific for VP6 can provide cognate help to B cells specific for neutralizing epitopes on the VP7 and/or VP4 molecules, and that this help can be heterotypic. Finally, we provide evidence that this phenomenon may be happening during infection.

High prevalence of serum antibodies to Ras and type 16 E4 proteins of human papillomavirus in patients with precancerous lesions of the uterine cervix.

Serum samples from 38 healthy women and 55 women with different types of cervical lesions were investigated for the presence of antibodies to Ras and against E4 and E7 proteins of human papillomavirus type 16 (HPV-16). Our results showed that anti-E7 antibodies were closely associated with cervical cancer (75%), as previously reported. Interestingly, E4 antibodies showed higher prevalence in condyloma lesions (79%; 11/14) than in cervical cancer (60%; 12/20). We also identified 11% (4/38) of healthy individuals as positive for E4 antibodies, which suggests an early immune recognition of this protein. Patients with condyloma and cervical intraepithelial neoplasia (CIN) also showed higher prevalences of Ras antibodies (approximately 40%) than cervical cancer patients (10%; 2/20). By sequencing part of the ras genes and using different Ras antigens, we showed that serum antibodies from patients were not directed to a Ras mutation, since wild-type cHa-Ras protein was recognized by these antibodies. In addition, patients positive for Ras antibodies (94%) were also positive for E4 antibodies, suggesting an association between these. The high prevalence of antibodies against Ras and E4 proteins in pre-malignant lesions opens the possibility of using both antibodies as early markers for potential cervical cancer patients.

Granulocyte colony-stimulating factor (G-CSF) transiently suppresses mitogen-stimulated T-cell proliferative response.

Granulocyte colony-stimulation factor (G-CSF) is a cytokine that selectively promotes growth and maturation of neutrophils and may modulate the cytokine response to inflammatory stimuli. The purpose of this study was to examine the effect of G-CSF on ex vivo peripheral blood mononuclear cell (PBMC) functions. Ten patients with breast cancer were included in a clinical trial in which r-metHuG-CSF was administered daily for 5 days to mobilize peripheral blood stem cells. Ten healthy women were also included as controls. Our data show that G-CSF treatment induces an increase in peripheral blood leucocyte, neutrophil, lymphocyte and monocyte counts. We have found a modulation in the percentages of CD19+, CD45+ CD14+, CD4+ CD45RA+ and CD4+ CD45RO+ cells in PBMC fractions during G-CSF treatment. We have also found a significant reduction in the proliferative response of PBMC to mitogenic stimulation that reverted 14 days after the fifth and the last dose of G-CSF. Furthermore, it was not associated with significant changes in the pattern of cytokine production. The mechanism of this immunoregulatory effect is probably indirect since G-CSF receptor has not been found in T lymphocytes. This mechanism and its potential clinical applications remain to be elucidated.

Defective proliferative response of T lymphocytes from patients with inactive systemic lupus erythematosus.

OBJECTIVE: To further define the pattern of alterations in the activation and apoptosis of T lymphocytes in patients with inactive systemic lupus erythematosus (SLE) through analysis of a large series of individuals. METHODS: We isolated CD2+ peripheral blood lymphocytes (PBL) from 41 patients with inactive SLE and analyzed their proliferative and apoptotic responses to polyclonal activation. RESULTS: In 19 of 41 (47%) patients, a low proliferative response to polyclonal mitogens was found. This defective response was inversely associated with an increased apoptotic response and increased expression of CD95 and CD45RO antigens. CONCLUSION: We found that 2 groups of patients with inactive disease can be defined according to the functional behavior of their T lymphocytes, as defined by the proliferative and apoptotic responses to mitogenic signals.

Immunological changes in peripheral blood mononuclear cells of patients with metastatic renal cell carcinoma after low doses of subcutaneous immunotherapy with IFN-alpha-2b and IL-2.

To elucidate the immunologic changes induced by low doses of subcutaneous interferon (IFN)-alpha-2b plus interleukin-2 (IL-2) in patients with metastatic renal cell cancer, we have studied a group of eight patients undergoing two cycles of immunotherapy after radical nephrectomy. Natural killer (NK) cytotoxic activity, proliferative response to T-lymphocyte mitogens, and phenotypic profile of T and NK cells were determined in peripheral blood mononuclear cells (PBMCs) before and after each cycle. No significant differences were found in either of the studies realized between untreated patients and their counterpart healthy controls. However, after the first cycle, there was a significant increase in NK-cytotoxic activity and in the number of CD16+/CD56+ cells that parallelled a significant decrease in the percentage of CD3+ and CD4+ lymphocytes with no changes in the proliferative response to T-cell mitogenic signals. Individual analysis of each patient on the basis of their clinical response to treatment showed that after the first cycle of immunotherapy there were no significant differences in the immunological profiles analyzed between patients with complete or partial responses and those who did not respond to treatment, whereas, at the end of the second cycle, patients who achieved complete or partial clinical responses had higher NK-cytotoxic activity that those who remained in disease progression. We conclude that subcutaneous immunotherapy with IFN-alpha-2b and IL-2 induces a systemic immunomodulatory effect on PBMCs, manifested preferentially in a systemic NK activation and expansion that is related to the clinical outcome.

Altered pattern of cytokine production by peripheral blood CD2+ cells from B chronic lymphocytic leukemia patients.

To determine if activation-induced cytokine production is altered in CD2+ lymphocytes from B-CLL patients, cytokine levels were determined by ELISA in supernatants of PHA-stimulated cultures of CD2+ cells from 33 B-CLL patients and 22 healthy controls. The production of Interferon gamma (IFN-gamma) and Tumor Necrosis Factor (TNF-alpha) by mitogen-activated CD2+ lymphocytes from B-CLL patients was higher than that found in healthy controls, while no differences were found in TNF-beta production. IFN-gamma and TNF-alpha levels determined at 72 h in PHA-stimulated CD2+ cell cultures from B-CLL patients statistically correlated with the percentages of CD3+CD45RO+ and CD3-CD56+ lymphocytes, respectively. Although there were differences in the production kinetics of interleukins (ILs) 2 and 4 between B-CLL patients and the healthy controls, no differences were found at the time when the levels of both interleukins peak. The production of both IFN-gamma and IL-4 by PHA-stimulated CD2+ lymphocytes from non-smouldering B-CLL patients was significantly higher than that from smouldering B-CLL patients while no significant differences were found in the production of IL-2, TNF-alpha, and TNF-beta between the two B-CLL patient groups. These data suggest that functional alterations in the production of cytokines by CD2+ cells from B-CLL patients could help to explain the expansion of leukemic cells in B-CLL patients.

[Cholestasis in pregnancy. Report of a case]. / Colestasis del embarazo. Presentación de un caso.

We present a case of Cholestasis and pregnancy that developed associated in the puerperium, to tecaluteinic ovaries and hemoperitoneum. For this reason it was necessary surgical management. We considered that it is a very unusual case so we felt interest on presenting it. To finish we would to make reference to itns possible patogenia, symptoms, and management of it.

Morphological variants of leukemic cells in B chronic lymphocytic leukemia are associated with different T cell and NK cell abnormalities.

B chronic lymphocytic leukemia (B-CLL) is a heterogeneous disease. The different morphological variants of leukemic B cells appear to define different clinical groups of patients. Several abnormalities have been found in T lymphocytes and natural killer (NK) cells from B-CLL patients. We have investigated the phenotypic and functional characteristics of purified CD2+ cells from B-CLL patients at Binet's stage A and classified according to the neoplastic B lymphocyte morphology criteria: 32 patients with typical B-CLL and 12 patients with atypical B-CLL. Forty-three age and sex matched healthy controls were also studied. In fresh purified CD2+ cells from typical B-CLL patients, percentages of CD4+, CD4+CD45RA+, CD8+CD45RA+ T lymphocytes and CD3-CD56+ (NK) cells were significantly higher than those found in atypical B-CLL patients. However, in DC2+ cells from typical B-CLL patients, percentages of CD3+, CD3+DR+, CD8+, CD4+CD45RO+, and CD3+CD56+ cells were significantly lower than those found in atypical B-CLL patients. Increased percentage of NK cells was only found in typical B-CLL patients. The proliferative response and the production of interleukin (IL)-2 and IL-4 by phytohemagglutinin (PHA) stimulated CD2+ cells were significantly higher in typical B-CLL patients than in atypical B-CLL patients. We concluded that different patterns of phenotypic and functional alterations in the T lymphocytes and NK cells of B-CLL patients are found in patients with typical or atypical B-CLL defined according to the morphology of the leukemic cells.

Identification of a T-helper cell epitope on the rotavirus VP6 protein.

In this work, we have studied the T-helper (Th)-cell response against rotavirus, in a mouse model. Adult BALB/c mice were inoculated parenterally with porcine rotavirus YM, and the Th-cell response from spleen cells against the virus and two overlapping fragments of the major capsid protein VP6 (VP6(1-192) and VP6(171-397)) were evaluated in vitro. The Th cells recognized the YM virus and the two protein fragments, suggesting that there are at least two Th-cell epitopes on the VP6 molecule. To study the specificity of Th cells against VP6 at the clonal level, we established two Th-cell hybridomas cross-reactive for the VP6 protein of rotavirus strains YM and SA11. Both hybridomas recognized the VP6(171-397) polypeptide, and a synthetic peptide comprising the amino acids 289 to 302 (RLSFQLVRPPNMTP) of YM VP6 in the context of the major histocompatibility complex class II IEd molecule. The Th-cell hybridomas recognized rotavirus VP6 in a highly cross-reactive fashion, since they could be stimulated by eight different strains of rotavirus, including the murine rotavirus EDIM, that represent five G serotypes and at least two subgroups. The amino acid sequence of the VP6 epitope is highly conserved in most group A rotavirus strains sequenced so far. On the other hand, it was found that Th cells specific for the VP6 epitope may constitute an important proportion of the total polyclonal Th-cell response against rotavirus YM in spleen cells. These results demonstrate that VP6 can be a target for highly cross-reactive Th cells.

Structure of the N-linked oligosaccharides of MHC class I molecules from cells deficient in the antigenic peptide transporter. Implications for the site of peptide association.

Class I molecules are N-linked glycoproteins encoded by the MHC. They carry cytosolic protein-derived peptides to the cell surface, displaying them to enable immune surveillance of cellular processes. Peptides are delivered to class I molecules by the transporter associated with Ag processing (TAP). Peptide association is known to occur before exposure of class I molecules to the medial Golgi-processing enzyme alpha-mannosidase II, but there is limited information regarding the location or timing of peptide binding within the earlier regions of the endoplasmic reticulum (ER)-Golgi pathway. A reported association of newly synthesized class I molecules with the ER chaperonin calnexin raises the possibility of persistence of the monoglycosylated N-linked oligosaccharide (NLO) Glc1Man8GlcNAc2, known to be recognized by this lectin. To explore these matters, we determined the structure of the NLOs on the subset of newly synthesized class I molecules awaiting the loading of peptide. We pulse-labeled murine MHC H-2Db class I molecules in RMA/S cells, which lack one of the TAP subunits, causing the great majority of the molecules to be retained for prolonged periods in an early secretory compartment, awaiting peptide binding. MHC molecules pulse-labeled with [3H]glucosamine were isolated, the NLOs specifically released and structurally analyzed by a variety of techniques. Within the chosen window of biosynthetic time, most Db molecules from parental RMA cells carried mature NLOs of the biantennary complex-type, with one to two sialic acid residues. In RMA/S cells, such chains were in the minority, the majority consisting of the precursor forms Man8GlcNAc2 and Man9GlcNAc2. No glucosylated forms were detected, nor were the later processing intermediates Man5-7GlcNAc2 or GlcNAc1Man4-5GlcNAc2. Thus, most Db molecules in TAP-deficient cells are retained in an early compartment of the secretory pathway, before the point of first access to the Golgi alpha-mannosidase I, which trims alpha 1-2 linked mannose residues, but beyond the point where the alpha 1-3-linked glucose residue is finally removed by the ER glucosidase II. Thus, structural analysis of NLOs on class I molecules within a defined biosynthetic window has established a biochemical measure of the timing of peptide association.

Assembly, intracellular localization, and nucleotide binding properties of the human peptide transporters TAP1 and TAP2 expressed by recombinant vaccinia viruses.

The transporter associated with antigen processing (TAP) transports short peptides from the cytosol to the endoplasmic reticulum, where peptides assemble with class I molecules of the major histocompatibility complex. TAP is comprised of two subunits, termed TAP1 and TAP2. We produced recombinant vaccinia viruses that direct synthesis of the TAP subunits, either individually or together. Virus-encoded TAP is rapidly and efficiently assembled (t1/2 of 5 min or less) by cells and does not spontaneously assemble in detergent extracts. By confocal immunofluorescence microscopy, TAP1 when expressed alone or with TAP2 is largely, if not exclusively, localized to the endoplasmic reticulum. Metabolic labeling with [2-3H]mannose demonstrates that TAP1 (but not TAP2) possesses Asn-linked oligosaccharides, but the lack of binding of [35S]methionine-labeled TAP to concanavalin A-agarose suggests that the glycosylated form represents a minor population of TAP1. The two subunits of the assembled complex present in detergent extracts photolabeled equally with 8-azido-[alpha-32P]ATP. Photolabeling of the two subunits was inhibited in parallel by various di- and trinucleotides, suggesting that their nucleotide binding sites function in a highly similar manner. Incubation of detergent extracts at 37 degrees C results in the rapid loss of TAP1 immunoreactivity, indicating either an unusual sensitivity to proteases or an irreversible conformation alteration.

Effect of TAP on the generation and intracellular trafficking of peptide-receptive major histocompatibility complex class I molecules.

Using a fluorescein-conjugated antigenic peptide, peptide-receptive H-2Kb MHC class I molecules were found throughout the secretory pathways of RMA cells and peptide transporter (TAP)-deficient derivative cells (RMA/S). RMA/S cells displayed higher levels of intracellular peptide-receptive molecules, while, surprisingly, RMA cells expressed 3- to 5-fold more cell surface peptide-receptive molecules. Metabolic radiolabeling of Kb-associated oligosaccharides with [1-3H]galactose demonstrated that despite a large difference in the fraction of Kb molecules in native conformation in detergent extracts, Kb transport rates from the trans-Golgi complex to the surfaces of RMA and RMA/S cells were similar. Thus, although considerable numbers of class I alpha chains reach the RMA/S cell surface, they are a less productive source of peptide-receptive molecules than class I molecules synthesized by TAP-expressing RMA cells, suggesting paradoxically that TAP functions to increase the amount of peptide-receptive molecules at the cell surface.

Molecular mechanisms used by tumors to escape immune recognition: immunogenetherapy and the cell biology of major histocompatibility complex class I.

In this article, we explore the hypothesis that tumor cells can escape recognition by CD8+ T cells via deficiencies in antigen processing and presentation. Aspects of the molecular and cellular biology of major histocompatibility complex class I are reviewed. Evidence for histology-specific molecular mechanisms in the antigen-processing and -presentation deficiencies observed in some human and murine tumors is presented. Mechanisms identified include down-regulation of antigen processing, loss of functional beta 2-microglobulin, and deletion of specific alpha-chain alleles. Finally, we discuss studies using an antigen-presentation-deficient mouse tumor as a model for the immunogenetherapy of an antigen-presentation deficiency.

Presentation of numerous viral peptides to mouse major histocompatibility complex (MHC) class I-restricted T lymphocytes is mediated by the human MHC-encoded transporter or by a hybrid mouse-human transporter.

The major histocompatibility complex-encoded transporter associated with antigen processing (TAP) is required for the efficient presentation of cytosolic antigens to class I-restricted T cells. TAP is thought to be formed by the interaction of two gene products, termed TAP1 and TAP2. We find that TAPs consisting either of human subunits, or mouse TAP1 and human TAP2, facilitate the presentation of numerous defined viral peptides to mouse class I-restricted T cells. As human and mouse TAP2 and TAP1 differ in 23 and 28% of their residues, respectively, this indicates that TAP1 and TAP2 can form a functional complex with partners considerably different from those they coevolved with. Moreover, these findings indicate that widely disparate TAPs facilitate delivery of the same peptides to class I molecules. These findings suggest that TAP polymorphism does not greatly influence the types of peptides presented to the immune system.

Identification of human cancers deficient in antigen processing.

Intracellular antigens must be processed before presentation to CD8+ T cells by major histocompatibility complex (MHC) class I molecules. Using a recombinant vaccinia virus (Vac) to transiently express the Kd molecule, we studied the antigen processing efficiency of 26 different human tumor lines. Three cell lines, all human small cell lung carcinoma, consistently failed to process endogenously synthesized proteins for presentation to Kd-restricted, Vac-specific T cells. Pulse-chase experiments showed that MHC class I molecules were not transported by these cell lines from the endoplasmic reticulum to the cell surface. This finding suggested that peptides were not available for binding to nascent MHC molecules in the endoplasmic reticulum. Northern blot analysis of these cells revealed low to nondetectable levels of mRNAs for MHC-encoded proteasome components LMP-7 and LMP-2, as well as the putative peptide transporters TAP-1 and TAP-2. Treatment of cells with interferon gamma enhanced expression of these mRNAs and reversed the observed functional and biochemical deficits. Our findings suggest that downregulation of antigen processing may be one of the strategies used by tumors to escape immune surveillance. Potential therapeutic applications of these findings include enhancing antigen processing at the level of the transcription of MHC-encoded proteasome and transporter genes.