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M R Szewczuk

Publications and source records attributed to M R Szewczuk.

At least 19 recordsLinked to original sources
PubMed1999

Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid.

All nucleated mammalian cells synthesize protoporphyrin IX (PpIX) when exposed to exogenous 5-aminolevulinic acid (ALA). The response to exogenous ALA under standard conditions (the ALA phenotype) is characteristic for each cell type. Significantly more PpIX accumulates in malignant and premalignant cells than in the normal cells from which they were derived. A rodent fibroblast model was developed to study the mechanisms responsible for this phenomenon. Exogenous ALA induced the accumulation of substantial concentrations of PpIX in fibrosarcoma cells, and in immortalized fibroblasts transfected with the oncogene c-myc, IGF-1 receptor, IGF-1 and its receptor, v-fos, v-raf, v-Ki-ras, v-abl, or polyomavirus middle T antigen with G418 resistance selection. Much lower concentrations of PpIX accumulated in primary fibroblast cultures, in immortalized fibroblast cell lines, and in immortalized fibroblasts transfected with the G418-resistance gene only. The mechanisms responsible for the increased accumulation of ALA-induced PpIX by transformed cells (the malignant ALA phenotype) therefore appear to be closely linked to the mechanisms responsible for malignant transformation. Identification of the nature of that linkage may lead to new approaches to cancer therapy.

3T3 Cells↗
PubMed1999

Effect of mammalian cell differentiation on response to exogenous 5-aminolevulinic acid.

Many different types of mammalian cells accumulate fluorescing and photosensitizing concentrations of protoporphyrin IX (PpIX) when exposed to exogenous 5-aminolevulinic acid (ALA) in vivo or in vitro. Most types of malignant cells accumulate substantially more ALA-induced PpIX than do the normal cells from which they arose. Most types of malignant cells also are less differentiated than their normal counterparts. We therefore considered the possibility that malignant cells demonstrate a malignant ALA phenotype (accumulate abnormally large amounts of PpIX when exposed to exogenous ALA) as a direct consequence of their less differentiated state. Human promyelocyte cell line HL-60 and mouse preadipocyte cell line 3T3 L1 were induced to differentiate by exposing them to inducing agents in vitro. The HL-60 cells accumulated less ALA-induced PpIX when differentiated, but the 3T3 L1 cells accumulated more. It appears then that changes in the ALA phenotype with changes in the state of differentiation are cell-type specific. The decreased accumulation of ALA-induced PpIX that accompanied differentiation of the promyelocytic leukemia cells may have clinical application for rapid quantitation of the response of myelocytic leukemia patients to differentiation therapy.

3T3 Cells↗
PubMed1994

Sinusoidal 60 Hz electromagnetic fields failed to induce changes in protein synthesis in Escherichia coli.

Escherichia coli JM83 [F- ara delta(lac-proAB) rpsL [phi 80d delta (lacZ)M15]] in midlog growth phase at 30 degrees C were exposed to 60 Hz sinusoidal magnetic field of 3 mT of nonuniform diverging flux, inducing a nonuniform electric field with a maximum intensity of 32 microV/cm using an inductor coil. Exposed and unexposed control cells were maintained at 30.8 +/- 0.1 degrees C and 30.5 +/- 0.1 degrees C, respectively. Quadruplicate samples of exposed and unexposed E. coli cells were simultaneously radiolabeled with 35S-L-methionine at 10 min intervals over 2 hr. Radiochemical incorporation into proteins was analyzed via liquid scintillation counting and by denaturing 12.5% polyacrylamide gel electrophoresis. The results showed that E. coli exposed to a 60 Hz magnetic field of 3 mT exhibited no qualitative or quantitative changes in protein synthesis compared to unexposed cells. Thus small prokaryotic cells (less than 2 microns x 0.5 micron) under constant-temperature conditions do not alter their protein synthesis following exposure to 60 Hz magnetic fields at levels at 3 mT.

Autoradiography↗
PubMed1992

Evidence for T lymphocyte reactivity to the 65 kilodalton heat shock protein of mycobacterium in active Crohn's disease.

The role of mycobacterial heat shock proteins (Hsp) of the 65 kilodalton Hsp family as a possible factor governing cell-mediated immune responses, leading to chronic mucosal inflammation, was examined. Purified peripheral blood mononuclear cells (PBMC) from patients with CD and ulcerative colitis (UC), and from healthy and disease controls were stimulated in culture with a highly purified, recombinant 65 kilodalton Hsp (rHsp65) of M. bovis BCG for 5 d. Cultures were then pulsed with 3H-thymidine for 24 h and uptake determined by liquid scintillation. We found that PBMC from patients with active CD exhibited a significant proliferative response to the soluble rHsp65 as compared with normal controls. In contrast, the proliferative responses of PBMC from patients with inactive CD, inactive and active UC, pancreatitis and cecal carcinoma were found to be not different from controls. Purified T cells or non-T cells of PBMC in the absence of antigen-presenting cells from active CD patients exhibited a lack of proliferative responses to the rHsp65 stimulation in culture. The data indicate an aberrant sensitization of T cells to the 65 kilodalton mycobacterial Hsp in a specific type of IBD, and thus may provide an important clue for the etiopathogenesis of Crohn's disease.

Adult↗
PubMed1992

Analysis of direct tissue isoelectric focused protein profiles of resected intestinal mucosa and endoscopic biopsies from patients with inflammatory bowel disease.

Direct tissue isoelectric focusing was used as a procedure to analyze differences in soluble tissue protein profiles of resected intestinal segments and endoscopic biopsies from patients with ulcerative colitis, Crohn's disease, and colonic cancer. Extraction of tissue proteins was accomplished by electrophoresis of mucosal cryostat sections on agarose gels across a broad pH gradient. The inflamed colonic mucosa from Crohn's disease patients showed similar isoelectric focusing protein patterns. Small bowel mucosa from a patient with both colonic diverticular disease and Crohn's disease showed protein patterns identical with that of the mucosa from a patient with only Crohn's disease. The inflamed mucosae from ulcerative colitis patients revealed identical protein patterns but were distinct from those of non-inflamed ulcerative colitis mucosa and from the inflamed mucosae from Crohn's disease patients. Non-inflamed small bowel mucosae from cancer, ulcerative colitis, and Crohn's disease patients showed distinct protein patterns which were absent in the non-inflamed large bowel mucosae. The inflamed resected ileum of a Crohn's disease patient exhibited protein patterns similar to those of the biopsy of an inflamed mid-transverse large bowel. Mucosal biopsies from inflamed sigmoid colon of a Crohn's disease patient showed different protein patterns than those in biopsies from the inflamed mid-transverse colon. Thus, distinctive isoelectric focusing protein patterns may be useful in differentiating Crohn's colitis and ulcerative colitis when granulomata are absent, and in resolving indeterminant colitis to one of these classic inflammatory bowel diseases.

Biopsy↗
PubMed1991

Bee venom anti-idiotypic antibody is associated with protection in beekeepers and bee sting-sensitive patients receiving immunotherapy against allergic reactions.

Bee venom (BV) anti-idiotypic (anti-Id) antibodies (Abs) were studied in nonreactive beekeepers, patients receiving BV immunotherapy (IT), and in patients with bee-sting hypersensitivity. Detection of serum anti-BV was determined either by the Phadebas RAST test for IgE and IgG concentrations or by isoelectric focusing followed by capillary blotting onto nitrocellulose membranes. Clonotypic analyses of Ab were made with specific probes for BV or BV anti-Id; 13/14 nonreactive multiple-sting beekeepers (93%; p = 0.00006) and 3/3 patients receiving BV IT (100%; p = 0.0026) had detectable amounts of BV anti-Id in serum, whereas five BV-sensitive patients (0%) and four ragweed-sensitive control patients (0%) did not. Beekeeper's serum containing BV anti-Id was found to recognize and bind to IgE anti-BV idiotype from two different patient sources and inhibit their reactions in a Phadebas RAST test in a dose-dependent manner. Nonreactive beekeepers generally had BV-specific IgE levels less than 0.35 PRU/ml in serum with detectable BV anti-Id. BV-allergic patients before IT had elevated BV-specific serum IgE levels, even in the presence of BV-specific IgG greater than 136 U/ml with no BV anti-Id present. These findings provide strong support for a protective role of BV anti-Id against bee sting--allergic reactions.

Adolescent↗
PubMed1991

Differential effect of aging on B-cell immune responses to cholera toxin in the inductive and effector sites of the mucosal immune system.

The age-associated primary immune response of B cells from the Peyer's patches (PP), the lamina propria (LP), the mesenteric lymph nodes (MLN), and the spleen of mice following oral immunization with cholera toxin (CTx) was investigated. The induction of immune responses was assessed in 4-, 11-, and 24-month-old, individual C57BL/6J male mice by determining the number and isotype of anti-CTx ELISPOT-forming cells (SFC) in the PP, LPL, MLN, and spleen and the titer and isotype of serum anti-CTx antibody. The data indicate a significant age-associated decline in immunoglobulin G (IgG) and IgA anti-CTx SFC in the LP B cells but only in IgA anti-CTx SFC in the PP. No decline was seen in the anti-CTx SFC response in the MLN and spleen. Peroral immunization of mice with CTx resulted in a serum anti-CTx antibody response which was predominantly of the IgG class in all three age groups of mice tested. There was no age-associated decline in anti-CTx IgM, IgG, or IgA titers in serum. Isoelectric focusing and affinity immunoblotting revealed several distinct new antibody clonotypes in the immune serum of old mice following oral immunization with CTx. The results indicate a loss of immune responsiveness to CTx following oral immunization in senescent PP and LP B cells. The MLN and spleen B-cell responses were found to be refractory to the loss of immune function with aging. These findings suggest a differential effect of aging in the inductive and effector sites of the mucosal immune system, and the loss of antigen-specific IgA responses at mucosal sites may have adverse effects on the host's defense against potential pathogens.

Administration, Oral↗
PubMed1989

Hapten-induced model of chronic inflammation and ulceration in the rat colon.

We have developed a simple and reproducible rat model of chronic colonic inflammation by the intraluminal instillation of a solution containing a "barrier breaker" and a hapten. Administration of the hapten 2,4,6-trinitrobenzenesulfonic acid (5-30 mg) in 0.25 ml of 50% ethanol as the "barrier breaker" produced dose-dependent colonic ulceration and inflammation. At a dose of 30 mg, trinitrobenzenesulfonic acid/ethanol-induced ulceration and marked thickening of the bowel wall persisted for at least 8 wk. Histologically, the inflammatory response included mucosal and submucosal infiltration by polymorphonuclear leukocytes, macrophages, lymphocytes, connective tissue mast cells, and fibroblasts. Granulomas were observed in 57% of the rats killed 3 wk after induction of inflammation. Langhan's-type giant cells were also observed. Segmental ulceration and inflammation were common. The characteristics and relatively long duration of inflammation and ulceration induced in this model afford an opportunity to study the pathophysiology of colonic inflammatory disease in a specifically controlled fashion, and to evaluate new treatments potentially applicable to inflammatory bowel disease in humans.

Animals↗
PubMed1988

T-cell immunoregulation in patients with inflammatory bowel disease. II. Enhanced suppressor T-cell activity in ulcerative colitis.

In a recent study, we have shown that peripheral blood B cells from patients with ulcerative colitis (UC) synthesized less immunoglobulin (Ig) in co-culture with autologous T cells than normal adults' B cells. When UC patients' T cells were co-cultured with normal adults' B cells, Ig synthesis was significantly decreased as compared with normal controls. In contrast, Crohn's disease (CD) patients' B and T cells functioned normally. In the present study, the activity of suppressor T cells in patients with UC and CD was determined. Peripheral blood B and T cells with monocytes were obtained from patients and normal adults of the same age and sex, and co-cultured for 10 days with pokeweed mitogen (PWM). Suppressor T-cell function was measured in mixed co-culture assays in which graded numbers of normal or patient's T cells were added to normal adults' B and T cells with PWM. Immunoglobulins (Ig) M, G and A were measured in culture supernatants using a sensitive enzyme-linked immunosorbent assay. The quantity of Ig present in the culture supernatants was determined from a standard curve. T cells from UC patients significantly decreased immunoglobulin production by control B and T cells (IgM and IgA, p = 0.02; IgG, p = 0.01). In contrast, addition of T cells from CD patients produced no significant differences. Complement mediated, monoclonal OKT8 antibody directed cell lysis revealed that the inhibition observed with UC patients' T cells in co-culture was due to a T8+ suppressor T cell. The degree of inhibition of immunoglobulin synthesis did not correlate with disease activity, duration of illness, location of disease, or corticosteroid treatment. Thus, patients with ulcerative colitis display enhanced suppressor T-cell activity in peripheral blood while patients with CD show normal helper and suppressor T-cell functions. These results provide evidence supporting a role for altered immunoregulatory activity in the pathogenesis of ulcerative colitis.

Adult↗
PubMed1988

T-cell immunoregulation in patients with inflammatory bowel disease. I. Differential helper T-cell function in ulcerative colitis and Crohn's disease.

The role of helper T-cells in patients with ulcerative colitis (UC) and Crohn's disease (CD) was investigated. Peripheral blood B- and T-cells with or without monocytes were obtained from patients and normal adults of the same age and sex, and co-cultured for 10 days with pokeweed mitogen (PWM). Immunoglobulins (Ig) M, G and A were measured in the culture supernatants using a sensitive enzyme-linked immunosorbent assay. The quantity of Ig present in the culture supernatants was determined from a standard curve. Immunoglobulins M, G and A synthesis and secretion by B-cells in the presence of T-cells required monocytes and PWM. The data indicate that co-cultures of heterologous normal adult T-cells and B-cells with PWM did not significantly affect Ig synthesis as compared with autologous cultures. Autologous cultures of CD patients' B- and T-cells were found not to be significantly different from normals in their capacity to synthesize Ig. In contrast, autologous UC patients' B- and T-cells were found to be significantly less effective as compared with normal adults' co-cultures in the synthesis Ig. When CD patients' T-cells were in co-culture with normal adults' B-cells, Ig synthesis was maintained. However, a marked diminution in Ig synthesis was seen when UC patients' T-cells were used in co-culture with normal adults' B-cells. The degree of inhibition of immunoglobulin synthesis did not correlate with disease activity, duration of illness, location of disease, or corticosteroid treatment. These results suggest that patients with ulcerative colitis have an altered helper T-cell population while CD patients' T-cells are either normal or hyperactive in the capacity to provide helper function in PWM-induced immunoglobulin secretion by peripheral blood B-cells.

Adult↗
PubMed1986

Analysis of serum antibody repertoires by isoelectric focusing and capillary blotting onto nitrocellulose paper.

A rapid method for the analysis of antigen-specific human serum antibodies is described. After isoelectric focusing on thin agarose gels, serum proteins are transferred to nitrocellulose paper by capillary blotting. The kinetics of transfer indicated that ca. 90% of 125I-labelled isolated human immunoglobulins (IgG, IgA and IgM) are transferred to the nitrocellulose paper within 10 min. Probing of the nitrocellulose blot with 125I-labelled tetanus toxoid antigen followed by autoradiography reveals the total serum anti-tetanus toxoid antibody repertoire, including high molecular weight IgM. This procedure is rapid (results can be obtained in less than 12 h), sensitive and should prove very useful for detailed studies and analysis of antibody repertoires in body fluids and extracts

Adult↗
PubMed1986

Natural killer cell activity in murine muscular dystrophy. III. NK-sensitive myoblast cells and lack of NK activity in beige/dystrophic hybrid mice.

The NK-susceptibility of dystrophic mouse myoblast cells was investigated. Spleen cells from 8- to 10-week-old normal (+/+) and dystrophic (dy2J/dy2J) male C57BL/6J mice were fractionated on Percoll density gradients and the cells at each density interface were incubated with either 51Cr-labeled YAC-1 or myoblast cells in a 6 hr 51Cr-release assay. Myoblast target cells were obtained from either heterozygous (+/dy2J) or homozygous (dy2J/dy2J) muscle cultures or a transformed tetraploid myoblast line (M14D2). The data indicate that the interface between the 50 and 60% (1.060-1.075 g/ml) Percoll density fractions of spleen cells from either normal or dystrophic mice contains the largest proportion of asialo GM-1 positive and NK-1 positive cells displaying NK activity. Myoblast cells from either heterozygous (phenotypically normal) or homozygous dystrophic mice were not significantly different in susceptibility to NK-mediated lysis by Percoll enriched normal or dystrophic mouse NK cells. However, dystrophic mouse spleen cells had the highest NK activity against both myoblast targets as compared with normal mouse spleen cells. The transformed myoblast cell line, M14D2, was significantly less susceptible to NK-mediated lysis by dystrophic mouse spleen cells when compared with freshly cultured myoblast target cells. Target cell binding studies revealed that conjugate forming cells from the 50% Percoll density interface of dystrophic mouse spleen cells were approximately twofold greater than that of normal mouse spleen cells against either heterozygous or homozygous dystrophic mouse myoblast targets. Cold target inhibition studies revealed that the natural killing of dystrophic mouse myoblast cells was due to a YAC-1 reactive NK cell. Breeding experiments between C57BL/6J homozygous "beige" (bgJ/bgJ) mutant mice and dystrophic (dy2J/dy2J) mice produced beige/dystrophic hybrid mice which displayed clinical symptoms of the dystrophy process by 3 to 4 weeks of age. Spleen cells from these hybrid mice showed no significant differences in NK activity against YAC-1 target cells when compared with homozygous beige mice. Taken together, these results demonstrate the first reported evidence that murine myoblasts are susceptible to NK-mediated lysis. In addition, the data indicate that although dystrophic mouse NK cells recognize myoblast cells as targets, the NK cell studies with the beige/dystrophic hybrid mice do not indicate a direct in vivo role for NK cells in the dystrophy process.

Animals↗
PubMed1986

Natural killer cells in murine muscular dystrophy. IV. Characterization of Percoll fractionated splenic and thymic natural killer cells and natural killer-sensitive thymocyte targets.

The Natural Killer (NK) activity in the thymus and NK-sensitive thymocyte targets of dystrophic mice was investigated. Dystrophic and normal mouse thymocytes or spleen cells were layered on discontinuous Percoll gradients (5 or 10% increments, respectively) between 40 and 70% and centrifuged at 1700 g for 30 min. All fractions were tested for either NK activity or used a 51Cr-labeled NK-sensitive targets in a 6-hr 51Cr release assay. The density interface between the 50% (1.060 g/ml) and 60% (1.075 g/ml) Percoll fractions of either dystrophic or normal mouse spleen cells and the 40% (1.050 g/ml) and 50% (1.060 g/ml) Percoll fractions of either dystrophic or normal mouse thymocytes were found to contain the largest proportion of NK activity using YAC-1 lymphoma tumor cells as targets. In addition, the NK activity in dystrophic mouse spleen cells and thymocytes was significantly greater when compared with normal mouse controls. Target binding cell studies revealed that these Percoll fractions of dystrophic mouse spleen cells and thymocytes had greater numbers of conjugate-forming cells when compared with normal control groups. Cell depletion experiments using either anti-Thy 1.2, anti-asialo-GM 1 or anti-NK-1 plus complement treatment revealed that the cell responsible for NK activity in the 50% Percoll fraction interface of dystrophic mouse spleen cells was asialo-GM 1 positive. NK-1 positive, and partially Thy 1.2 positive. However, the cells displaying NK-activity in the thymus of normal or dystrophic mice were found to be highly Thy-1.2 positive and peanut agglutinin (PNA) negative. The density interface between the 60% (1.075 g/ml) and 65% (1.081 g/ml) Percoll fractions of either normal or dystrophic mouse thymocytes contained the largest proportion of NK-sensitive target cells. Interestingly, the 60% Percoll fraction of dystrophic mouse thymocyte targets was significantly more susceptible to NK-mediated lysis than that of the normal mouse thymocyte population. Cell depletion experiments revealed that the NK-sensitive thymocyte population was similar in both mice, that is, Thy-1.2 positive, cortisone sensitive, PNA positive, Dolichos biflorus (DBA) negative and asialo GM-1 negative. The results indicate that there are density differences between splenic and thymic NK cells. In addition, there are density and phenotypic differences between thymic NK cells and thymic NK-sensitive target cells. The findings support the hypothesis that there are different populations of NK cells.

Animals↗
PubMed1985

Age-related strain differences in the development of auto-anti-idiotypic antibody regulation in the splenic and mucosal-associated lymphoid systems.

In the present study, we examined the changes that occur with age in anti-idiotype-blocked, hapten-augmentable PFC in the mucosal-associated lymph nodes (MLN and BLN) and spleen of various strains of mice. 2-month-old 129/J, AKR/J, and C57L/J mice had a high percentage of hapten-augmentable PFC in their spleen, MLN, and BLN; however, by 6-11 months these values had declined considerably in the spleen, while mucosal values remained high. In contrast, 2-month-old C57BL/6J, DBA/2J, and C3H/HeJ mice had a low percentage of hapten-augmentable PFC in their spleen, MLN, and BLN; but by 6-11 months these values had increased considerably in the spleen, while mucosal values remained low. CBA/J and SJL/J mice maintained high and low levels, respectively, of hapten-augmentable PFC in their spleens, MLN, and BLN over the age span. NZB/BinJ mice were found to be low producers in the spleen, but high in the MLN and BLN at 2 and 6 months of age. These data indicate that there are strain differences in the development of auto-anti-idiotypic antibody regulation with age.

Aging↗
PubMed1984

Strain differences in the development of auto-anti-idiotypic antibody regulation with age: genetic linkage to the Igh-C locus.

The effect of age on the appearance of anti-idiotype (Id)-blocked, hapten-augmentable plaque-forming cells (PFC) in various strains of mice was investigated. Strains of mice at 2 and 6-11 months of age were immunized with 500 micrograms trinitrophenylated bovine gamma-globulin (TNP-BGG) in complete Freund's adjuvant (CFA) intraperitoneally. Splenic IgM and IgG anti-TNP PFC responses were assayed for anti-Id-blocked, hapten-augmentable PFC 14 days after immunization. It was found that strains differ with regard to the age at which they produce anti-Id-blocked, hapten-augmentable PFC. C57BL/6J (B6), DBA/1J, and C3H/HeJ mice produced a significantly high percentage of hapten-augmentable IgG anti-TNP PFC at 8-9 months of age as compared with the 2-month-old group. In contrast, 129/J, AKR/J, and C57L/J mice produced a significantly low percentage of hapten-augmentable PFC at 6-7 months of age as compared with the 2-month-old group. The CBA/J mice were high-hapten-augmentable plaque producers at both 2 and 7 months of age. SJL/J mice were, on the other hand, low producers at 2 and 11 months of age. Immune sera from high hapten-augmentable plaque-producing strains caused a hapten-reversible block of plaque formation by spleen cells from TNP-BGG-immune C57BL/6J mice and also revealed anti-(anti-TNP F(ab')2-IgG) titer as assayed by passive hemagglutination. This PFC-inhibiting activity in the immune sera of old C57BL/6J mice was an antibody of the IgG2a and IgG3 classes, lacked anti-TNP antibody activity, but reacted with anti-TNP antibody of C57BL/6J origin. Genetic analysis between high hapten-augmentable plaque production and allotypes in the (129/J X B6) crosses of the same H-2b haplotypes revealed that all of the backcrosses and F2 with high hapten-augmentable plaque production had the Igh-1a allele of the high-producer, 129/J mouse. In contrast, the crosses with low hapten-augmentable plaque production were homozygous for the Igh-1b allele of the low-producer, B6 mouse. The data suggest strain differences in the development of auto-anti-idiotypic antibody regulation with age which may be controlled by a gene(s) linked to the Igh-C locus.

Aging↗
PubMed1984

Natural killer (NK) cell activity in murine muscular dystrophy. II. Age-related tissue distribution and enhanced NK activity in the thymus of dystrophic mice.

The age-related tissue distribution of natural killer (NK) cell activity in murine muscular dystrophy was investigated. Lymphoid tissues including the spleen, thymus, mediastinal (or bronchial) lymph nodes (BLN), mesenteric lymph nodes (MLN), inguinal/popliteal lymph nodes (PLN1), and axillary/brachial lymph nodes (PLN2) were obtained from various aged normal (+/+) and dystrophic (dy2J/dy2J) C57BL/6J mice. Cell suspensions were incubated with 51Cr-labeled YAC-1 lymphoma target cells in a 4-hr 51Cr-release assay. The data indicated that dystrophic mice, at all ages studied, had elevated levels of NK activity in the spleen, BLN, MLN, PLN1, and PLN2 as compared with the normal age- and sex-matched control group. The NK activity in the thymocyte population from dystrophic mice at 2 weeks of age was found to be negligible, while at 8 weeks of age it was two-fold higher than that for the normal control group. In addition, dystrophic mice had an age-related decline in NK activity in all tissues after 10 weeks of age but the activity was still elevated at 40 weeks of age as compared with the normal control group. Target cell binding studies revealed that the number of conjugate-forming cells in thymocytes from 8-week-old dystrophic mice were found to be significantly higher than that found in normal mouse thymocytes using NK-sensitive YAC-1 tumor target cells. The number of cells bound per YAC-1 target cell ranged from 1 to 3 for dystrophic mouse thymocytes as compared with 1 to 2 for the normal control group. Thus, the data indicate an elevated NK activity in all lymphoid tissues studied from dystrophic mice of different ages. In addition, the thymus from dystrophic mice at 8 weeks of age contains an enhanced number of conjugate-forming NK cells and NK activity.

Aging↗