PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Local Lymph Node Assay”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources

Detection of clinically significant, occult prostate cancer metastases in lymph nodes using a splice variant-specific rt-PCR assay for human glandular kallikrein.

PURPOSE: To compare the detection of human glandular kallikrein 2 (hK2) mRNA expression in archival lymph nodes with disease progression, the development of prostate cancer metastases, and mortality in patients undergoing radical prostatectomy for locally advanced nonmetastatic prostate cancer. PATIENTS AND METHODS: We evaluated total RNA extracted from fixed, paraffin-embedded, histopathologically normal pelvic lymph nodes, removed at radical prostatectomy, from 199 pT3N0 prostate cancer patients (150 extraprostatic extension only; 49 seminal vesicle involvement) for hK2-expressing cells using a novel reverse transcriptase polymerase chain reaction (RT-PCR)/hK2 assay. Cumulative incidence functions and Cox proportional hazards analyses were performed. RESULTS: Forty patients (20%) had positive results, 80 patients (40%) had negative results, and 79 patients (40%) had equivocal results. RT-PCR/hK2 status was not associated with any pathologic characteristics (P >.05). In postoperative multivariable models, the RT-PCR/hK2 result was associated with prostate cancer progression (P =.001), development of distant metastases (P =.001), and prostate cancer-specific survival (P =.005). In patients experiencing biochemical progression (n = 33), RT-PCR/hK2 status was a predictor of failure to respond to salvage radiotherapy (P =.002). CONCLUSION: RT-PCR/hK2 can detect biologically and clinically significant occult prostate cancer metastases in histopathologically normal lymph nodes. In patients with locally advanced prostate cancer, RT-PCR/hK2 is strongly associated with prostate cancer progression, failure following salvage radiation therapy, development of clinically evident metastases, and prostate cancer-specific mortality after surgery.

Aged↗

Prognostic significance of urinary antigen analysis by enzyme-linked immunosorbent assay in melanoma patients.

Urine samples collected from normal donors and melanoma patients were analyzed for the presence of tumor-associated antigen by competitive inhibition in the enzyme-linked immunosorbent assay (ELISA) using an allogeneic melanoma serum as the source of antibody and partially purified urine from the same donor as the target antigen. The results were expressed as antigen units (ng antigen protein/mg creatinine). The antigen levels in urine of melanoma patients (median = 56.5, N = 56) were significantly higher (P less than 0.05) than those of normal donors (median = 1.9, N = 56). The 90th percentile for the normal group was 34.3 antigen units. Using this value as the criterion for positivity, 36 of 56 (64%) urine samples of melanoma group were positive for the antigen as opposed to only 6 of 56 (11%) of normal donors. Subsequently, a retrospective analysis of 58 melanoma patients paired on the basis of disease recurrence and no recurrence after lymphadenectomy revealed a median antigen level of 68 units for the recurrent group and 18.9 for the nonrecurrent group. Eighteen of 29 (62%) melanoma patients who had recurrence of their disease and 9 of 29 (31%) patients who remained disease free were urinary antigen positive. These incidences were significantly different (P less than 0.005). The results of this investigation suggest that assessment of urinary antigen in stage I and II melanoma patients may prognosticate recurrence of the disease.

Antigens, Neoplasm↗

Fluorescence in situ hybridization and immunohistochemical assays for HER-2/neu status determination: application to node-negative breast cancer.

BACKGROUND: HER-2/neu (ERBB2) gene amplification and/or overexpression is a major event in human breast tumorigenesis. HER-2/neu gene alterations have been the most frequently assessed prognostic factors during the last 10 years in breast cancer and have recently emerged as a management decision tool and a therapeutic target. There is still controversy over the best method to determine whether a tumor is HER-2/neu positive. Because of the increasing demand for HER-2/neu gene status determination in clinical practice, we compared HER-2/neu gene alterations at the DNA level (gene amplification) and the protein level (overexpression) in a panel of patients with lymph node-negative breast cancer who had received local radiotherapy alone, with no adjuvant therapy. METHODS: We tested 100 excised lymph node-negative breast tumors, using fluorescence in situ hybridization (FISH) with a biotinylated HER-2/neu DNA probe and immunohistochemical assays (IHC) with 2 different antibodies. RESULTS: The FISH frequency of HER-2/neu gene amplification was 15%, and the IHC frequency of overexpression was 21%. CONCLUSION: Although HER-2/neu amplification by FISH and HER-2/neu overexpression by IHC correlated well in this panel of lymph node-negative breast carcinomas, there were a number of discordant cases, pointing to the important need for determining HER-2/neu alteration for the future management of HER-2/neu-based clinical applications.

Adult↗

Expression of the DNAM-1 ligands, Nectin-2 (CD112) and poliovirus receptor (CD155), on dendritic cells: relevance for natural killer-dendritic cell interaction.

In this study, we demonstrate the involvement of DNAM-1-triggering receptor and its ligands, poliovirus receptor (PVR) and Nectin-2, in natural killer (NK) cell-mediated lysis of dendritic cells (DCs). The surface expression of both ligands was up-regulated in DCs as compared to monocytes. It reached maximal densities after DC maturation induced by different stimuli including lipopolysaccharide (LPS), poly I:C, flagellin, and CD40L. Both immunohistochemical analysis and confocal microscopy revealed expression of DNAM-1 ligands by DCs in lymph nodes in which they were localized in the parafollicular T-cell region and surrounded the high endothelial venules. Remarkably, in cytolytic assays, DNAM-1 cooperated with NKp30 in the NK-mediated killing of both immature and mature DCs and the degree of contribution of DNAM-1 appeared to correlate with the surface densities of its specific ligands PVR and Nectin-2.

Antigens, Differentiation, T-Lymphocyte↗

TRAF-4 expression in epithelial progenitor cells. Analysis in normal adult, fetal, and tumor tissues.

TRAF-4 was discovered because of its expression in breast cancers and is a member of the tumor necrosis factor (TNF) receptor-associated factor (TRAF) family of putative signal-transducing proteins. In vitro binding assays demonstrated that TRAF-4 interacts with the cytosolic domain of the lymphotoxin-beta receptor (LT beta R) and weakly with the p75 nerve growth factor receptor (NGFR) but not with TNFR1, TNFR2, Fas, or CD40. Immunofluorescence analysis of TRAF-4 in transfected cells demonstrated localization to cytosol but not nucleus. Immunohistochemical assays of normal human adult tissues revealed prominent cytosolic immunostaining in thymic epithelial cells and lymph node dendritic cells but not in lymphocytes or thymocytes, paralleling the reported patterns of LT beta R expression. The basal cell layer of most epithelia in the body was very strongly TRAF-4 immunopositive, including epidermis, nasopharynx, respiratory tract, salivary gland, and esophagus. Similar findings were obtained in 12- to 18-week human fetal tissue, indicating a highly restricted pattern of expression even during development in the mammary gland, epithelial cells of the terminal ducts were strongly TRAF-4 immunopositive whereas myoepithelial cells and most of the mammary epithelial cells lining the extralobular ducts were TRAF-4 immunonegative. Of 84 primary breast cancers evaluated, only 7 expressed TRAF-4. Ductal carcinoma in situ (DCIS) lesions were uniformly TRAF-4 immunonegative (n = 21). In the prostate, the basal cells were strongly immunostained for TRAF-4, whereas the secretory epithelial cells were TRAF-4 negative. Basal cells in prostate hypertrophy (n = 6) and prostatic intraepithelial neoplasia (PIN; n = 6) were strongly TRAF-4 positive, but none of the 32 primary and 16 metastatic prostate cancer specimens examined contained TRAF-4-positive malignant cells. Although also expressed in some types of mesenchymal cells, these findings suggest that TRAF-4 is a marker of normal epithelial stem cells, the expression of which often ceases on differentiation and malignant transformation.

Adult↗

Immunohistochemical detection of Yersinia pestis in formalin-fixed, paraffin-embedded tissue.

Yersinia pestis infection usually is limited to lymph nodes (bubo); rarely, if bacteria are aerosolized, pneumonic plague occurs. We developed an immunohistochemical assay using a monoclonal anti-fraction 1 Y pestis antibody for formalin-fixed tissues. We studied 6 cases using this technique. Respiratory symptoms were prominent in 2 cases; histologically, one showed intra-alveolar inflammation, and the other had alveolar hemorrhage and edema. By using the immunohistochemical assay, we found intact Yersinia and granular bacterial antigen staining in alveoli, bronchi, and blood vessels. Of the remaining cases, 2 had septicemia and 2 had a bubo. Pathologic changes included lymphocyte depletion, necrosis, edema, and foamy macrophages in lymph nodes; multiple abscesses in the spleen; fibrin thrombi in glomeruli; and unremarkable lungs. By using the immunohistochemical assay, we identified intact bacteria inside monocytes and granular antigen staining in blood vessels. The immunohistochemical assay provided a fast, nonhazardous method for diagnosing plague. The immunohistochemical assay localizes bacteria, retaining tissue morphologic features, and can help define transmission mechanisms.

Adolescent↗

Systemic and mucosal immune responses to H1N1 influenza virus infection in pigs.

Influenza is a common respiratory disease in pigs, and since swine influenza viruses are zoonotic pathogens, they also pose human health risks. Pigs infected with influenza virus mount an effective immune response and are protected from subsequent challenge, whereas the currently available, inactivated-virus vaccine does not consistently confer complete protection to challenge. To develop and evaluate new vaccination strategies, it is imperative to fully understand the immune responses that are associated with protection following natural infection. Therefore, we have evaluated the phenotype and kinetics of immune responses to primary and re-challenge infection with H1N1 swine influenza virus in the pig. Through the use of isotype-specific antibody secreting cell ELISPOT assays, interferon-gamma ELISPOT assays and isotype-specific ELISAs on serum, nasal wash and bronchoalveolar lavage samples, we defined the humoral and cellular immune responses, both locally in the respiratory tract and systemically, to this viral infection. Virus-specific serum IgG, IgA, and HI titers all peaked 2-3 weeks after primary infection and did not substantially increase after re-challenge. The predominant virus-specific isotype in serum was IgG. Pigs responded with virus-specific IgG and IgA in both the upper (nasal washes) and lower (bronchoalveolar lavages) airways; IgA was the predominant isotype in both sites. Despite the fact that the pigs were completely protected from re-challenge, the antibody titers in the nasal washes increased. Results of the antibody-secreting cell ELISPOT assays demonstrated that the numbers of both IgG and IgA secreting cells in the nasal mucosa were dramatically higher than in any other tissue examined. In contrast, IFN-gamma secreting cells were predominantly localized to the spleen and tracheobronchial lymph nodes. These data will be helpful in the future development and evaluation of novel vaccines.

Animals↗

Activation of CD4+ and CD8+ lymphocyte subsets by streptozotocin in the popliteal lymph node assay. II. Comparison with acute graft-vs-host reaction in H-2 incompatible F1 mouse hybrids.

Changes in lymphocyte subsets during an acute GVH reaction were compared to STZ-induced PLN response in mice. The GVH reaction was induced locally by sc injection of parental C57Bl/6 [B6] spleen cells into (C57Bl/6 x DBA/2) F1 footpad [B6D2F1]. Early cell activation and time-related changes in T- and B-lymphocyte subsets were monitored during the onset of the GVH reaction by flow cytometry and immunophenotyping. Examination of cell size and chromatin decondensing for T- and B-cell subsets showed differences in activation profile during the early phase of the GVH reaction. The present study provides direct evidence for early in vivo activation of both CD4+ and CD8+ T-cells. Our data confirm the central role of T-cell activation in the induction of a GVH reaction and suggest that recirculatory host B-cells can play an important role in early GVH node enlargement. Overall, our comparative analysis supports the concept of polyclonal T-cell activation for both STZ-related and GVH-induced lymphoproliferation. Chemicals-induced lymphoproliferation leading to autoimmune reactions is a challenging issue. A number of drugs and chemicals have been tested in the PLNA assay for lymphoproliferative potential. We previously reported the activation and proliferation of T-cell subsets following STZ injection into murine footpads. The STZ-induced PLN enlargement and proliferation characteristics of T- and B-cell subsets were postulated to be similar to those of an acute allogeneic GVHR. In the present study, a cytometric analysis of T- and B-cell subsets in PLNs was performed during an acute allogeneic GVHR, for comparison purposes. Such a reaction results in a massive node enlargement five to ten times that seen after stimulation with conventional antigens. Acute GVHR is believed to be a direct consequence of the high frequency of alloreactive donor T-cells inducing a massive proliferation of B-cells, almost exclusively of host origin, in GVHR nodes. It is now widely accepted that donor T-cells activated as the result of exposure to foreign MHC antigens in the recipient, secrete various cytokines which assist the host B-cells and bypass the normal B-T cell cooperation. Induction of an acute GVHR, as in the parental B6--->recipient B6D2F1 model, requires the injection of CD4+ and CD8+ donor T-cells into an F1 recipient that differs from the parent at both MHC class I and II loci.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Selective stimulation of cutaneous interleukin 6 expression by skin allergens.

Epidermal cells, both keratinocytes and Langerhans cells, are able to synthesize and secrete a variety of cytokines, many of which influence or are essential for the induction of skin sensitization and the elicitation of local inflammatory reactions. It has been proposed that it may prove possible to distinguish between contact allergens and skin irritants as a function of differential induction or upregulation of epidermal cytokine expression. In the present study we have addressed this by examination of the local cutaneous production of interleukin 6 (IL-6) following topical exposure of mice to oxazolone, a potent contact allergen, or to benzalkonium chloride (BZC), a skin irritant that is considered not to have a significant potential to cause skin sensitization. Both oxazolone and BZC could induce the production of IL-6 as measured by enzyme-linked immunosorbent assay in homogenates prepared from treated skin. However, when these chemicals were applied at concentrations that resulted in equivalent cutaneous inflammatory responses, based on induced oedema, only oxazolone provoked the production in skin of IL-6. Moreover, under these conditions exposure only to oxazolone resulted in the secretion by draining lymph node cells of measurable concentrations of this cytokine. These data suggest that the ability of oxazolone to stimulate local IL-6 production is not secondary simply to the induction of local inflammatory responses. As such, the results support the possibility that skin allergens and skin irritants may stimulate variable patterns of epidermal cytokine production.

Adjuvants, Immunologic↗

[Immunity of the skin--infection and percutaneous immunization of rabbits with E. coli ATCC 13676].

After intracutaneous infection of rabbits with a suspension of E. coli which was followed by a transient local inflammation, the local and systemic immune responses were determined using the lymphocyte stimulation test (LTT) and the hemolysis plaque assay (HPA). Lymphocytes of the lymphatic system draining the infected skin area and blood lymphocytes were used. With lymphocytes derived from the local lymph nodes, a substantial increase of specific stimulation in the LTT was detected beginning at day 3 after infection and lasting up to the termination of the experiment (3 weeks). Blood lymphocytes were stimulated at a lower level: The activity showed a peak at day 4 and an elevated level only during a 10-day period. After the intracutaneous infection with E. coli, increasing numbers of antibody-releasing lymph node cells were detected in the HPA. The antibody-secreting cells of the IgM and IgG classes clearly showed an increasing specificity for E. coli lipopolysaccharide coupled to sheep red blood cells. As with the LTT, the highest activities (values of specificity and number of plaque-forming lymphocytes) were observed at the end of the experimental period. An emulsified preparation of a heat-inactivated E. coli culture (E. coli-BKS) which had been applied locally onto the artificially altered skin evoked a similar immunological response after a 2 or 3-weeks treatment. In such animals an increased activity of lymph node cells could be registered by LTT and HPA as compared to reactions from placebo-treated control animals. However, the topical immunization with nonviable E. coli stimulated not only lymphocytes which produced antibodies directed specifically against E. coli lipopolysaccharide as demonstrated by the HPA. An increased number of lymphocytes reacted even with native sheep red blood cells. This observations is discussed in respect of a polyclonal B-cell activation by lipopolysaccharide of the E. coli-BKS.

Animals↗

Detection of metastatic prostate cancer using a splice variant-specific reverse transcriptase-polymerase chain reaction assay for human glandular kallikrein.

We developed a highly sensitive splice variant-specific reverse transcriptase-PCR (RT-PCR) assay for human glandular kallikrein (hK2) mRNA and tested its ability to detect metastatic disease in men with clinically localized prostate cancer. An RT-PCR assay using primers spanning intron IV and including a significant portion of the 3' untranslated region of the hKLK2 gene, with maximum nonhomology to both hK1 and hK3, was developed. The limit of detection of the assay was five copies of hK2 cDNA and one LNCaP cell in 10(9) lymphoblasts. RT-PCR-hK2 was performed on preoperative peripheral blood specimens from 228 consecutive radical prostatectomy patients as well as 7 metastatic prostate cancer patients and 14 healthy men without prostate cancer. This new RT-PCR-hK2 assay amplifies two distinct fragments. The larger fragment (hK2-U) is approximately 680 bp in length and corresponds to the amplified product of a previously reported splice variant in the splice donor site of intron IV in the hKLK2 gene. The smaller fragment (hK2-L) is approximately 643 bp in length and corresponds to the amplified product of the native hK2 mRNA. Whereas the RT-PCR-hK2-L assay was positive in 71% of our patients with metastatic prostate cancer, 14% of healthy control men also tested positive. By univariate (P = 0.028) and multivariate (P = 0.0269) analysis, which controlled for preoperative PSA, clinical stage, and biopsy Gleason score, RT-PCR-hK2-L status added prognostic information to the prediction of lymph node-positive disease. We have developed a new RT-PCR assay which demonstrates a high sensitivity for detecting hK2 mRNA. Preoperative RT-PCR-hK2-L status helps predict pathological lymph node positivity in patients with clinically localized prostate cancer.

Adult↗

Transient early metabolic and functional hyperreactivity and late areactivity of lymphocytes in preleukemic AKR mice.

The dynamics of changes in the metabolic and functional activities of thymus, lymph node and spleen lymphocytes and spleen macrophages of AKR mice was examined during the preleukemic period. The MTT colorimetric assay was used to determine the mitochondrial enzyme activity of viable cells, the local xenogeneic GVH reaction and the IL-2 assay for measuring T cell responses, and the IL-1 assay as an indicator of macrophage activity. In the early preleukemic period (at 1.5 months of age), lymphocyte dehydrogenase enzyme hyperactivity was accompanied by a highly increased production of IL-2, positive local xenogeneic GVH reaction and increased IL-1 production. Later on, at the age of 4-5 months, AKR mice demonstrated a progressive decrease in the metabolic activity of lymphocytes, negative local GVH reaction and reduction or lack in IL-2 and IL-1 production. This early hyperreactivity and late, gradually evolving, areactivity of lymphocytes and macrophages was not found in other, non-leukemic strains of mice (RFM, CBA, C57BL).

Animals↗

Histological studies of bovine herpesvirus type 4 infection in non-ruminant species.

The pathology of bovine herpesvirus type 4 (BHV-4) infection was studied in cats, rabbits and guinea pigs. Twenty kittens, twenty-two rabbits and ten guinea pigs, some treated with glucocorticoid-were inoculated with a BHV-4 strain of feline origin, via various routes of inoculation (conjunctival, intranasal, peritoneal). Clinical signs were recorded. After euthanizing at different post inoculation days macro- and microscopic changes were observed by necropsy and in hematoxylin-eosin stained histological sections. The presence of the virus in organs was detected by immunohistochemistry and a nested PCR assay. Inclusion bodies and monoclonal antibody-stained cells were found in the conjunctiva, trachea, lungs, spleen and lymph nodes. Most of the lesions were localized to the respiratory and the immune system. The macro- and microscopic lesions and clinical signs were more severe in kittens and guinea pigs. The histological data indicated that cats, especially kittens, were susceptible for BHV-4 and the infection was not confined to the urinary bladder.

Animals↗

Development of a murine lymphoma model system for the characterization of natural killer:tumor cell interactions.

We have developed a model system which can be utilized for characterizing both the molecular basis of natural killer (NK):tumor interactions and the consequences of these interactions on tumor growth in vivo. This model system consists of several tumor lines which were derived from the murine lymphoma ASL1w under conditions which permitted the isolation of clonal lines that differ in their susceptibility to NK-mediated lysis. The NK-resistant clones used in this study (AW5J and AW5E) were susceptible to cytotoxic T-lymphocyte-mediated lysis and thus appear to be resistant to lytic processes utilized uniquely by NK cells. In competitive (cold target) inhibition assays, the AW5J clone did not inhibit NK recognition as well as the NK-sensitive clones. Thus AW5J may not be efficiently recognized by NK cells. The AW5E clone, on the other hand, competitively inhibited NK recognition as efficiently as the NK-sensitive clones; therefore, AW5E appears to evade a post-recognition event which is required for NK-mediated lysis. The susceptibility of these clones to killing by NK cells directly correlated with their lethality, suggesting that NK cells regulated the growth of these tumors in vivo. The level of host NK activity was also an important determinant of the level and site of tumor localization. Two-step immunofluorescence assays and flow cytometric analysis were used to quantitate the number of tumor cells in the bone marrow, spleen, and lymph nodes of mice with augmented or depleted NK activity. Increasing host NK activity decreased the number of tumor cells in each organ which could support the growth of the particular tumor tested. Furthermore, the extent of NK regulation was dependent, in part, upon the susceptibility of the particular tumor to NK-mediated lysis and the site of tumor growth. Thus, the data presented here demonstrate the utility of the ASL1w-derived clones as a model system which can be used to delineate the requirements and consequences of NK:tumor interactions.

Animals↗

Cell-mediated immune response to herpes simplex virus: type-specific lymphoproliferative responses in lymph nodes draining the site of primary infection.

Cell-mediated immune responses to type 1 and type 2 HSV were studied in rabbits using an in vitro lymphocyte transformation assay. The footpad route of inoculation was used to allow us to study the specificity and degree of localization of the responses. Rabbits inoculated in the hind footpads with infectious HSV-I or HSV-II mount type-specific lymphocyte transformation responses that are localized to draining lymphoid organs. Type-specificity requires careful control of all in vitro culture conditions and reflects the extensive cross-reactivity demonstrated by serologic techniques. While lymphocyte transformation responses can be detected with immune SL and PBL, presumably the result of early escape of antigen into the systemic circulation, responses by draining LNL are significantly greater in magnitude. Distant LNL have not been shown to respond. It is postulated that the augmented local immune response to HSV plays a significant role in controlling recurrent HSV infections.

Animals↗

The effects of cyclosporin on lymphocyte activation in a systemic graft-vs.-host reaction.

We have investigated the effects of cyclosporin (CsA) on each of three stages of lymphocyte activation in vivo viz. sequestration of alloantigen-reactive lymphocytes from the circulation into the spleen and lymph nodes, blast transformation and induction of DNA synthesis in the activated cells and release of these cells and their progeny into the circulation. Parental strain lymphocytes injected i.v. into semi-allogeneic rats and recovered from the thoracic duct within 36 h are profoundly unresponsive in a local graft-vs.-host assay to the alloantigens of the F1 hybrid but have normal activity against unrelated alloantigens (negative selection). CsA treatment of the F1 hybrid recipients did not prevent this selective sequestration of antigen-reactive cells. In the untreated F1 hybrid, from 36 h after injection, large numbers of dividing blast cells were released into the lymph. These cells did not appear in the lymph of recipients treated with CsA. However, CsA did not prevent the activation of cells sequestered in the spleen or lymph nodes as assessed by [3H] thymidine incorporation and autoradiography. This unexpected finding suggests that CsA inhibits lymphocyte responses to alloantigens in vivo after DNA synthesis which is a later stage than the in vitro studies have shown.

Animals↗

Effects of tumor growth on interleukins and circulating immune complexes. Mechanisms of immune unresponsiveness.

This study delineates the temporal relationship between immune complex formation and tumor growth, and provides one possible explanation for host immunosuppression during tumor growth. The authors have studied serial circulating immune complex (CIC) levels and interleukin (IL) elaboration by peripheral blood cells (IL-1 production by adherent mononuclear cells [AMC]; and IL-2 generation by peripheral blood mononuclear cells [PBMC]) during the growth of syngeneic tumor isografts in an inbred rat model. Male Wistar/Furth (W/Fu) rats were injected, subcutaneously (SC) with 2 X 10(6) W163 ( a dimethylhydrazine [DMH]-induced colon adenocarcinoma) cells into their hind limbs. Serial CIC levels, (measured by the antigen nonspecific polyethylene glycol turbidity assay) and IL-1 and IL-2 production were measured before isografting and weekly thereafter. Progressive local tumor growth occurred for 3 weeks followed by regional lymph node metastases during the fourth week. During local tumor growth, there was a progressive rise in CIC levels (123% rise compared with baseline value; P less than 0.05) which correlated with a fall in both IL-1 and IL-2 generation (r = -0.768). At the time of regional metastasis, the mean CIC levels declined, and there was a further significant decrease in IL production (IL-1 = 0.9% and IL-2 = 10% of controls in tumor bearers). These results show that progressive tumor growth results in decreased IL production by host PBC, and suggest that CIC may be involved in regulating IL generation.

Adenocarcinoma↗

Cell-mediated immune response in rotavirus-infected calves: leucocyte migration inhibition assay.

The cell-mediated immune (CMI) response was determined in rotavirus-infected calves by leucocyte migration inhibition assay with blood, spleen, mesenteric lymph node and intestinal lymphocytes. The inhibition of migration was more prominent in intestinal and mesenteric lymph node lymphocytes than in spleen and blood. In rotavirus-infected calves, the assay indicated the presence of CMI response which was more prominent at the local site of infection.

Animals↗