Biomedical subjects

M Alvarez-Mon

Publications and source records attributed to M Alvarez-Mon.

At least 37 records · Page 2Linked to original sources

PubMed1999

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.

Adult↗

PubMed1999

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.

Aged↗

PubMed1999

Factors mediating the hemodynamic effects of tumor necrosis factor-alpha in portal hypertensive rats.

Nitric oxide, prostacyclin, and glucagon have been implicated in promoting the hyperdynamic circulatory state of portal hypertension. Recent evidence also indicates that increased tumor necrosis factor-alpha (TNF-alpha) production is involved in the pathogenesis of this hemodynamic abnormality. This study was aimed at investigating in rats with portal vein stenosis (PVS) the effects on splanchnic hemodynamics of blocking circulating TNF-alpha and the factors mediating the vascular action of this cytokine in this setting. Anti-TNF-alpha polyclonal antibodies or placebo was injected into rats (n = 96) before and 4 days after PVS (short-term inhibition) and at 24 h and 4, 7, 10 days after PVS (long-term inhibition). Short-term TNF-alpha inhibition reduced portal venous inflow and cardiac index and increased splanchnic and systemic resistance. Portal pressure was unchanged, but portal-systemic shunting was decreased. After long-term TNF-alpha inhibition, portal venous inflow and portal pressure were unchanged, but arterial pressure and systemic resistance rose significantly. Anti-TNF-alpha PVS rats exhibited lower increments of systemic resistance after Nomega-nitro-L-arginine methyl ester and indomethacin administration and lower serum levels of TNF-alpha, nitrates-nitrites, and 6-keto-PGF1alpha, both over the short and the long term. Serum glucagon levels rose after long-term inhibition. In conclusion, the specific role played by TNF-alpha in the development of the hyperdynamic state of portal hypertension appears to be mainly mediated through an increased release of nitric oxide and prostacyclin. Maintenance of the splanchnic hyperemia after long-term TNF-alpha inhibition could be due to a compensatory release of glucagon.

Animals↗

PubMed1999

Regulatory effects of cytokines and cyclosporine A on peripheral blood mononuclear cells from stable multiple sclerosis patients.

The proliferative response (PR) of peripheral blood mononuclear cells (PBMC) to lectins such as phytohemaglutinin (PHA), anti-CD3 monoclonal antibodies such as OKT-3 or phorbol esters such as tetradecanoyl-phorbol 13-acetate (TPA) was investigated in 18 stable multiple sclerosis (MS) patients (9 untreated and 9 treated patients) and 10 healthy controls. PBMC from untreated MS patients showed a significantly higher PR to PHA than healthy controls. The PR of PHA, anti-CD3 or TPA stimulated PBMC from treated patients was lower than that from untreated MS patients. Mitogen stimulated PBMC from untreated patients shown both increased sensitivity to the stimulatory effect of IL-2 and increased resistance to the inhibitory effect of IL-10 and IFN-alpha. The addition of IL-2 increased the PR in PHA-stimulated PBMC from untreated MS patients, but not in those from treated MS patients and healthy controls. Mitogen stimulated cells from untreated patients were more resistant to the inhibitory effect of IL-10 and IFN-alpha than PBMC from either treated MS patients or healthy controls. Cyclosporine A (CsA) inhibited the PR and the expression of activation antigens induced by PHA in PBMC from the three groups of subjects. This inhibitory effect of CsA have was enhanced by the addition of IFN-alpha.

Adult↗

PubMed1999

Abnormal functional behavior of peripheral blood mononuclear cells from Hashimoto's disease patients. Immunomodulatory effects of cyclosporin A.

In vitro studies of activation and proliferation induced by mitogens in the presence of Cyclosporin A (CsA) and or cytokines were carried out to determine the effects of CsA and cytokines on mitogen activated peripheral blood mononuclear cells (PBMC) from thirteen Hashimoto's disease patients (HP) and ten healthy controls. The proliferative response (PR) of PBMC from HP to mitogens at 7 days of culture was higher than in controls. Interleukin 2 (IL-2) addition significantly increased the PR in phytohemagglutinin-stimulated PBMC from HP, but not in controls. CsA inhibited in a dose dependent manner the PR, as well as the expression of activation antigens induced by mitogens in both groups of subjects, but PBMC from HP were sensitive to CsA at lower doses than those that were effective on PBMC from controls. Both IL-2 or IL-4 overcame the inhibitory effect of CsA on PBMC from HP and controls. Conversely, IL-10 or IFN-alpha addition increases the inhibitory effect of CsA on the PR of PBMC from both HP and controls. We conclude that PBMC from Hashimoto's disease patients shown an abnormal pattern of PR that is associated to increased PR to mitogens and higher sensitivity to immunomodulatory effects of IL-2 and CsA.

Adjuvants, Immunologic↗

PubMed1999

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.

Adolescent↗

PubMed1998

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.

Adult↗

PubMed1998

Selective impairment of endothelium-mediated vasodilation in liver transplant recipients with cyclosporin A-induced hypertension.

Arterial hypertension is commonly observed in orthotopic liver transplantation (OLT) recipients receiving cyclosporin A (CsA), but the precise pathogenetic mechanisms remain partially unknown. The aim of this study was to investigate endothelium-dependent and -independent dilation and adrenergic constriction of resistance vessels of OLT recipients treated with CsA. Vascular reactivity was examined in 22 OLT patients, 10 with and 12 without arterial hypertension, and in 10 control subjects by assessing the forearm blood flow response to the brachial artery infusion of increasing concentrations of methacholine chloride, sodium nitroprusside, and phenylephrine. In 10 OLT patients, the response to methacholine was also examined after acetylsalicylate. The ratio of serum nitrite and nitrate to serum creatinine was lower (P < .05) in OLT patients with hypertension than in nonhypertensive patients and controls. Basal forearm flow was similar in the three groups. Methacholine vasodilation was impaired in the hypertensive patients as shown by a lower maximum forearm vasodilator response and a shift in the dose response curve to methacholine to the right compared with the nonhypertensive OLT patients and the controls. The response to methacholine was not modified after salicylate. Forearm flow response to nitroprusside was similar in the three groups. No differences between the patients and the controls were found in the maximum forearm flow contraction in response to phenylephrine. An impairment in endothelium-dependent vasodilation could mediate arterial hypertension in OLT patients immunosuppressed with CsA.

Adult↗

PubMed1998

[Evaluation of the hemodynamic effects of tumor necrosis factor alpha factor in rats with portal hypertension using the radioactive microsphere technique].

UNLABELLED: This study was aimed at investigating the effects of blocking circulating TNF on the hyperdynamic circulatory state developed in rats with portal vein stenosis (PVS), and the factors mediating the hemodynamic action of this cytokine in this setting. MATERIALS AND METHODS: Murine antiTNF polyclonal antibodies (100 microgram) or placebo were intravenously injected into PVS rats (n = 24) before and 4 days after PVS. Hemodynamic studies were performed the day after the last antiTNF injection. RESULTS: Short-term TNF inhibition led to reductions in cardiac index (p < 0.05) and portal venous inflow (p < 0.01), and significant increases in splanchnic and systemic vascular resistances. Portal pressure was unchanged, but portal-systemic shunting was decreased (p < 0.05). CONCLUSION: TNF plays a key role in promoting the development of the hyperdynamic state of portal hypertension. The effect of TNF is mediated through an increased release of nitric oxide.

Animals↗

PubMed1998

[Hepatitis B virus and the inflammatory/immunologic response (II): a new opportunity for the treatment of chronic hepatitis B and a suggestion for the treatment of other persistent viral diseases].

With the immunologic rationale exposed in the first part of this paper, the authors analyze a new experimental treatment which includes the combination of an antiviral (ribavirin) and an immunomodulator (AM3) in a model of hepatotoxic viral-infection in mice. Rationale for this associated treatment is based on the ability of AM3 to restore the natural immunity through the induction of IL-12 and IFN-gamma. Furthermore, the treatment with AM3 decreases factor C3 of the complement system which appears to be implied in IL-12 downregulation. Experimental and clinical results showed herein suggest a new approach to the treatment of viral hepatitis which combines the use of antivirals in combination with immunomodulators able to restore the "immunologic chaos" induced by some viruses.

Adjuvants, Immunologic↗

PubMed1997

Characteristics of thoracic duct lymph in multiple organ dysfunction syndrome.

OBJECTIVE: To investigate the presence of endotoxin, bacteria, and potential humoral and cellular mediators in thoracic duct lymph and peripheral blood in patients with severe refractory multiple organ dysfunction. DESIGN: Convenience sample. SETTING: General intensive care unit of a university hospital. PATIENTS: Two men and 2 women were studied after a mean of 7.25 days (range, 6-9 days) of multiple organ dysfunction syndrome. The primary injury was thoracic in 1 patient and abdominal in 3 patients. INTERVENTION: The thoracic duct was cannulated with a 7F catheter and samples of lymph and peripheral blood were obtained. MAIN OUTCOME MEASURES: Simultaneous lymph and serum levels of lipopolysaccharide, tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6, and activation markers on T lymphocytes. RESULTS: Lipopolysaccharide and cytokine levels were low in lymph and serum, except for a mean lymph-to-serum ratio of 53.4 for interleukin-1 beta. There was phenotypical evidence of intense polyclonal T-lymphocyte activation in both lymph and peripheral blood with increased lymph-to-peripheral blood ratios. Increased percentages in lymph of CD45RA + CD45RO + lymphocytes were observed. In 1 patient, Proteus mirabilis grew simultaneously in lymph, pancreatic necrosis fluid, and a central venous catheter tip. All simultaneous blood cultures were negative. CONCLUSIONS: Our results provide evidence of the participation of the gut-associated lymphatic tissue in the pathogenesis of the multiple organ dysfunction syndrome, suggesting that T-cell activation and cytokine production occur at the gut level. Future studies are needed to confirm and extend our findings.

Female↗

PubMed1997

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.

Adult↗

PubMed1997

Decreased natural killer cytotoxic activity in chronic alcoholism is associated with alcohol liver disease but not active ethanol consumption.

Chronic alcohol intake is associated with an increased incidence of certain neoplasms. Natural killer (NK) cells have been considered to be involved in control tumor development and growth. The goal of the present study was to contribute to a better understanding of the effects of ethanol (EtOH) per se on the NK-cell population. Both patients with chronic alcoholism without liver disease (AWLD) and subjects with alcohol-induced cirrhosis (ALC) were carefully selected for this study. Immunophenotypical and functional studies of peripheral blood (PB) NK-cells were performed during active EtOH intake and after 3 months of a withdrawal period. In the AWLD group a significant increase in number of NK-cells (CD3-/CD56+) (P < .05) associated with a parallel increase in NK-cell lytic activity (P < .01) was observed. In addition, the number of cytotoxic T cells displaying the CD3+/CD56+ phenotype as well as CD8-/CD57+ NK-cell subset was also increased (P < .01 and P < .001, respectively). By contrast, in ALC patients with active EtOH intake (ALCET group), although a significant increase in the number of NK PB lymphocytes was observed (P < .05), NK lytic activity was depressed (P < .05), suggesting the existence of a decreased lytic activity/NK-cell. After 3 months of EtOH withdrawal, PB mononuclear cells (PBMC) from the AWLD group patients still displayed an increased NK cytolytic activity; in addition, the number of PB NK-cells (CD3-/CD56+ and CD8-/CD57+) and CD3+/CD56+ PB T cells continued to be increased. Independently of the duration of withdrawal period, in ALC patients EtOH withdrawal was followed by a slight decrease in the NK lytic activity of PBMC with respect to the values in active alcoholism phase; slight differences observed in the NK lytic activity in ALC patients who quit drinking could be related to the tendency to decrease of the number of NK-cells toward normal values. Furthermore, although an increase in NK cytotoxic activity after stimulation of PBMC with interleukin-2 (IL-2) was observed in ALC, it did not reach the levels observed in healthy subjects. Overall, our results show that the behavior of PB NK-cell population in chronic alcoholism is different according to both the moment of EtOH consumption and the existence or not of ALC. Alcohol by itself induced an increase in the number and lytic activity of NK-cells. By contrast, the NK cytolytic activity is constantly depressed in the stage of alcoholic cirrhosis, supporting the notion that immunosurveillance mechanisms may be affected in these patients.

Adult↗

PubMed1997

An extract of the fern Polypodium leucotomos inhibits human peripheral blood mononuclear cells proliferation in vitro.

An alcoholic extract of the fern polypodium leucotomos (PLE) has been empirically used as an immunosuppressor for the treatment of several autoimmune diseases. In this paper, we investigated the effects of PLE on activation and proliferative responses of peripheral blood mononuclear cells (PBMNC) from healthy donors to T lymphocyte polyclonal mitogens. PLE shows a significant inhibitory effect on the proliferative response of PBMNC to stimulation with phytohaemagglutinin (PHA) or anti CD3 monoclonal antibodies (p < 0.05). In contrast, PLE did not modify the proliferative response of PBMNC to phorbol esters (p > 0.05). The inhibitory effect of PLE upon mitogen induced PBMNC proliferation is time dependent and can be overcome by the exogenous addition of interleukin-2 to the culture medium (p < 0.05). The decreased proliferative response of PBMNC to PHA stimulation in the presence of PLE is not associated with a significant modification of expression of the alpha chain (CD25) of the IL-2 receptor (p > 0.05). In conclusion, PLE shows an inhibitory effect on the polyclonal proliferative response of PBMNC to T lymphocyte mitogens that interact with cytoplasmic membrane molecules.

Adult↗

PubMed1997

Thymostimulin increases natural cytotoxic activity in patients with breast cancer.

The effect of thymostimulin on the Natural Killer (NK) cytotoxic activity of peripheral blood mononuclear cells (PBMC) was investigated in 15 patients with breast cancer after finishing or during chemotherapy (CAF) and in 10 healthy controls. PBMC from these subjects were incubated in the presence of thymostimulin for varying periods of time (18 h or 5 days), and then used as effector cells against 51Cr-radiolabeled NK-sensitive (K-562) and NK-resistant (JY) target cells in cytotoxicity assays. No significant differences were observed between the NK-activity from breast cancer patients and healthy controls. Thymostimulin induced a dose- and time-dependent cytotoxic enhancing effect on the cytotoxic activity of PBMC from these patients against NK-sensitive K562 target cells. The thymostimulin (1000 ng/ml) significantly enhanced cytotoxic activity in PBMC from breast cancer patients who had previously received chemotherapy (p = 0.0277) against NK-sensitive cells. This increase was not statistically significant neither in PBMC from patients receiving chemotherapy nor in healthy controls (p > 0.05 in both cases). The incubation of PBMC from patients with breast cancer was not associated to a significant enhancement of the cytotoxic activity against NK-resistant target cells (p > 0.05). We also found that thymostimulin could synergize with interleukin-2 in inducing NK cytotoxic activity in PBMC after 18 h of culture (p = 0.0277). In conclusion, we have demonstrated that thymostimulin enhances the natural killer cytotoxic activity of PBMC from patients with breast cancer who have previously received chemotherapy.

Adjuvants, Immunologic↗

PubMed1997

Prophylactic intracavitary treatment with interferon alpha increases interferon gamma production by peripheral blood mononuclear cells in patients with superficial transitional cell carcinoma of the bladder.

The immunomodulatory effect of prophylactic intravesical instillations of interferon alpha 2b (IFN-alpha-2b) on interferon gamma (IFN-gamma) and interleukin 4 (IL-4) production by peripheral blood mononuclear cells (PBMCs) from patients with superficial transitional cell carcinoma (STCC) of the bladder has been analysed. There were no significant differences in the production of IFN-gamma and IL-4 by PBMCs from untreated patients and healthy control subjects after 24 h of phytohaemagglutinin (PHA) stimulation. However, between 3 and 6 months after finishing the prophylactic intracavitary treatment with IFN-alpha-2b, PHA-stimulated PBMCs from patients with STCC of the bladder showed a significantly enhanced production of IFN-gamma and a significantly decreased production of IL-4. Both IFN-gamma and IL-4 returned to pretreatment levels 1 year after ending the treatment. In conclusion, prophylactic intravesical instillations of IFN-alpha-2b in patients with STCC of the bladder have an immunoregulatory effect on the production of IFN-gamma and IL-4 by PBMCs.

Adjuvants, Immunologic↗

PubMed1997

Cytokine levels after open and laparoscopic cholecystectomy.

A prospective study of serum cytokine levels was performed in patients randomly assigned to undergo either laparoscopic cholecystectomy (LC) or open cholecystectomy (OC). The kinetics of serum interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10), and cortisol were studied in both groups of patients. Cytokine and cortisol levels were measured in serum samples from patients who underwent either LC (n = 14) or OC (n = 14) using enzyme-linked immunosorbent assay and radioimmunoassay, respectively. Serum samples were obtained 24 h before surgery and 24 h and 7 days after surgery. IL-6 levels differed significantly (p < 0.05) between the LC and OC groups. IL-1 beta, IL-10, TNF-alpha and cortisol levels showed no significant differences (p > 0.05). Kinetic studies of IL-6, IL-1 beta and TNF-alpha levels revealed them to behave similarly, 24 h after surgery the levels of these cytokines were higher than those 24 h before surgery. These levels normalized by 7 days after surgery. Cytokine concentrations were always higher in the OC group than in the LC group. IL-1 beta and IL-10 levels were the most stable in both groups, though cortisol levels were also fairly stable.

Adult↗

PubMed1997

T lymphocytes infiltrating the bladder wall of patients with carcinoma of urinary bladder are in vivo activated.

OBJECTIVES: This paper studies the phenotypical characteristics of the lymphocytes present in mononuclear cell (MNC) preparations from peripheral blood (PBMNC), lymph nodes (LNMNC), tumor bladder (TBMNC), and tumor-free bladder (TFBMNC) from patients with infiltrated transitional cell carcinoma (TCC) of the bladder and PBMNC of healthy controls. METHODS: Eight patients diagnosed with TCC of the bladder, according to UICC criteria, and 10 healthy controls were studied. For immunofluorescence staining, T lymphocytes were incubated with combinations of fluorescein (FITC, green)- and phycoerytrin (PE, red)-labelled monoclonal antibodies. RESULTS: The percentage of NK cells in the LNMNC and TFBMNC was significantly decreased in comparison to that found in the PBMNC from these patients (p < 0.05). A significant enhancement of the expression of class II molecules of the major histocompatibility complex (MHC) by CD3+ T lymphocytes from TBMNC and TFBMNC specimens from bladder walls was found with respect to those quantified in CD3+ T lymphocytes from PBMNC (p < 0.05). In addition, the percentage of CD3+CD25+ T lymphocytes was significantly higher in PBMNC in TCC patients than in healthy controls (p < 0.05). CONCLUSIONS: Our data clearly demonstrate that the presence of infiltrative TCC of the bladder is associated to an infiltration of in vivo activated T lymphocytes of the urinary bladder wall. This in vivo T lymphocyte activation has been considered an expression of the immune response against the tumor cells.

Aged↗