Biomedical subjects

J R Gordon

Publications and source records attributed to J R Gordon.

At least 19 recordsLinked to original sources

PubMed1998

Experimental murine Trypanosoma congolense infections. II. Role of splenic adherent CD3+Thy1.2+ TCR-alpha beta- gamma delta- CD4+8- and CD3+Thy1.2+ TCR-alpha beta- gamma delta- CD4-8- cells in the production of IL-4, IL-10, and IFN-gamma and in trypanosome-elicited immunosuppression.

Trypanosome-induced suppression of T and B cell responses to parasite-related and -unrelated Ags is considered a major mechanism of evasion of the host's immune defenses by the parasite. Reduced T and B cell responses have been attributed to suppressor T cells, suppressor macrophages, or both. We have previously shown that endogenously produced IL-10 and IFN-gamma mediate the suppression of T cell responses in Trypanosoma congolense-infected mice. Here, we show for the first time that splenic CD3+ Thy1.2+ alphabeta- gammadelta- CD4+ 8- and CD3+ Thy1.2+ alphabeta- gammadetla- CD4- 8- cells that copurify with plastic-, nylon wool-, or Sephadex G-10-adherent cell populations, in synergy with adherent Thy1.2- cells, are the major producers of IL-4, IL-10, and IFN-gamma in T. congolense-infected mice. We further demonstrate the involvement of these cells in the suppression of T cell proliferative responses to mitogen and in B cell responses to a parasite-unrelated Ag.

Animals↗

PubMed1998

Experimental murine Trypanosoma congolense infections. I. Administration of anti-IFN-gamma antibodies alters trypanosome-susceptible mice to a resistant-like phenotype.

The mechanisms regulating resistance or susceptibility to African trypanosomes have been enigmatic. In this study, we assessed the production of several cytokines (IL-4, IFN-gamma, and TNF-alpha) in vivo and in vitro using genetically susceptible (BALB/c) or resistant (C57BL/6) mice infected with cloned Trypanosoma congolense and the role of these cytokines in pathogenesis of this infection. Plasma of infected BALB/c mice contained higher levels of IL-4 and IFN-gamma than the plasma of infected C57BL/6 mice. Conversely, plasma TNF-alpha levels were elevated significantly in the resistant mice relative to the susceptible ones. Splenic IFN-gamma mRNA appeared earlier and were maintained at higher levels in infected BALB/c than in C57BL/6 mice. Both spontaneous and Con A-induced secretions of IL-4 and IFN-gamma by splenocytes from infected BALB/c mice were significantly higher than those from their C57BL/6 counterparts. Con A-induced proliferation of splenocytes from infected BALB/c mice was progressively suppressed. Nitric oxide was not involved in this suppression, but the suppression was positively correlated with IFN-gamma secretion. Addition of neutralizing Abs to IFN-gamma to cultures of Con A-stimulated spleen cells from infected BALB/c mice effectively reversed this suppression. Furthermore, administration of anti-IFN-gamma Abs to BALB/c mice early during infection dramatically shifted the phenotype of these susceptible mice to a more resistant-like phenotype, as expressed by a low and undulating parasitemia and a >300% increase in survival period. These results strongly suggest that the enhanced induction and secretion of IFN-gamma during T. congolense infections contribute to the relative susceptibility of BALB/c mice to the disease.

Animals↗

PubMed1998

Elevation in tumour necrosis factor-alpha (TNF-alpha) messenger RNA levels in the uterus of pregnant gilts after oestrogen treatment.

In pigs, induction of embryonic degeneration, by exogenous oestrogens given early in gestation, has been long recognised. However, the underlying mechanisms responsible for this degeneration remain unclear. The present study was conducted to determine whether oestrogen-induced early porcine embryonic mortality was associated with changes in the levels of tumour necrosis factor-alpha (TNF-alpha) messenger RNA in the uterine endometrium. Prepubertal gilts were induced into oestrus with PG600 and artificially inseminated at their second natural oestrus and again 24 h later. After insemination, gilts were randomly assigned to treatment and given 0.5 ml intramuscular injections of either oestradiol valerate (10 mg ml-1) or corn oil on day 9 and 10 of gestation. The gilts were slaughtered on day 12, 15 or 18 of gestation. The reproductive tract was removed from each gilt and the uterine horns were flushed to check for the presence and integrity of embryos. Samples of uterine endometrial tissues were collected, snap-frozen in liquid nitrogen and stored at -80 degrees C. Total cellular RNA was isolated from frozen tissues using a guanidine isothiocyanate-cesium chloride method. The abundance of TNF-alpha messenger RNA was determined by Northern blot hybridisation analysis. Treatment of pregnant gilts with oestrogen resulted in severe fragmentation of embryos on days 15 (2/3) and 18 (2/2), confirming the embryocidal effect of exogenous oestrogen. Uterine TNF-alpha messenger RNA level was elevated in oestrogen-treated gilts compared with controls (P < 0.05). This observation of an association between increased levels of TNF-alpha mRNA in the uterus and embryonic degeneration in oestrogen-treated gilts suggests that TNF-alpha may be involved in mediating oestrogen-induced early embryonic mortality in the pig.

Animals↗

PubMed1998

Immunoregulation in experimental murine Trypanosoma congolense infection: anti-IL-10 antibodies reverse trypanosome-mediated suppression of lymphocyte proliferation in vitro and moderately prolong the lifespan of genetically susceptible BALB/c mice.

We infected highly susceptible BALB/c and relatively resistant C57BL/6 mice with cloned Trypanosoma congolense and followed the effects of these infections on the circulating parasite numbers, mouse mortality and cytokine expression. C57BL/6 mice controlled their parasitaemia and survived for up to 163 +/- 12 days, while BALB/c mice could not control their parasitaemia and succumbed to the infection within 8.4 +/- 0.5 days. Susceptible BALB/c mice had dramatically higher plasma levels of IL-10 than the resistant C57BL/6 mice from day 7 forward. This was preceded by an earlier and higher level induction of splenic IL-10 messenger RNA (mRNA) expression in the infected BALB/c mice. There was a strong negative correlation between the splenocyte proliferative responses to Concanavalin-A (Con-A) and their production of IL-10 in these infected BALB/c mice. Co-treatment of the Con-A-stimulated spleen cell cultures with monoclonal anti-IL-10 antibodies, but not isotype-matched control antibodies, could completely reverse this suppression of the splenocyte proliferative response. Finally, in three experiments, anti-IL-10 antibody treatment in vivo reduced the peak circulating parasitaemia of infected BALB/c mice by 43% and increased their median survival periods by 38% relative to isotype-matched control antibody-treated mice.

Animals↗

PubMed1998

Expression of the neutrophil chemoattractant interleukin-8 in the lesions of bovine pneumonic pasteurellosis.

We investigated the expression of interleukin-8 (IL-8) in pneumonic pasteurellosis of cattle because neutrophils are important mediators of tissue injury in this disease and because IL-8 is a major neutrophil chemoattractant in other species. We also compared IL-8 expression in bacterial and viral pneumonia, since the latter lacks the severe neutrophil exudation typical of pneumonic pasteurellosis. IL-8 expression was assessed by northern analysis, in situ hybridization, enzyme-linked immunosorbent assay, and in vivo bioassay. IL-8 mRNA expression was elevated dramatically in lesions of pneumonic pasteurellosis compared to unaffected lung from the same calves. In situ hybridization revealed intense expression of IL-8 mRNA in alveolar macrophages and neutrophils and milder expression in bronchiolar and alveolar epithelium, interstitial cells, and pleural mesothelium. Bronchoalveolar lavage fluid from lesional lung contained 16.06+/-4.00 ng/ml IL-8, whereas those from nonlesional and normal lung contained 0.34+/-0.11 and 0.01+/-0.002 ng/ml, respectively. We detected IL-8 expression at only minimal levels in bovine respiratory syncytial viral pneumonia. Lung extracts from lesions of pneumonic pasteurellosis induced vigorous neutrophil infiltration following injection into bovine skin, and 89% depletion of IL-8 from the extract reduced this neutrophil influx by 60%. These results demonstrate consistent upregulation of IL-8 expression in lesions of pneumonic pasteurellosis, implying a role for IL-8 in the ongoing recruitment of neutrophils to established lesions of pneumonic pasteurellosis. Because neutrophil-mediated tissue injury is critical to the pathogenesis of pneumonic pasteurellosis, these data suggest that neutralization of IL-8 activity could ameliorate the severe clinical signs and lesions of this disease.

Animals↗

PubMed1998

Relapse prevention as an interventive model for HIV risk reduction in gay and bisexual men.

Despite considerable self-initiated HIV risk reduction among men who have sex with men, little is known about how to design interventions that will effectively assist individuals from this population in maintaining safer sex behaviors over time. The present study evaluated the effectiveness of a 17-session group counseling intervention that incorporated components based on a cognitive-behavioral model of relapse. Differential behavioral outcomes following treatment included an increase in the percentage of sexual activities that were protected and a decrease in unprotected oral sex. However, considerable risk reduction (e.g., increased condom use, decreased unprotected sex, and decreases in the number of male partners and in the total number of sexual acts) occurred in both treated and untreated participants. Measures of mediating attitudinal variables drawn from relapse prevention theory largely predicted behavioral changes. Over time, several of the risk reduction behaviors achieved at posttreatment were not maintained, suggesting the importance of further developing effective strategies for supporting behavior change maintenance.

Adult↗

PubMed1997

Promotion of mouse fibroblast proliferation by IgE-dependent activation of mouse mast cells: role for mast cell tumor necrosis factor-alpha and transforming growth factor-beta 1.

Pathologic fibroblast proliferation or tissue fibrosis develops in certain chronic allergic diseases and in a wide array of other inflammatory disorders in which mast cell activation is also a prominent feature. In this study we investigated a number of potential mechanisms by which IgE-dependent activation of mouse mast cells might influence the proliferation of mouse fibroblasts in vitro. We found that supernatants from in vitro-derived mast cells that had been activated by IgE and specific antigen (but not those from quiescent mast cells) promoted the proliferation of mouse embryonic skin or 3T3 fibroblasts, and we showed that this effect was detectable in the absence of fetal calf serum. We analyzed the kinetics with which the fibroblast-proliferative activity was secreted from bone marrow-derived cultured mast cells and found that it was released both rapidly (i.e., in 30 minutes or less) and for a more prolonged period (i.e., for more than 2 hours) after IgE-dependent mast cell activation. We then measured the levels at which the mast cells produce a number of cytokines that are known to affect fibroblasts (IL-1, IL-6, transforming growth factor-beta 1 [TGF-beta 1], and tumor necrosis factor-alpha [TNF-alpha]) and assessed their relative effects, as recombinant cytokines, on fibroblast proliferation. Our mast cells secreted high levels of TGF-beta 1 and TNF-alpha, intermediate amounts of IL-6, and low levels of IL-1. We titrated the fibroproliferative effects of each of these cytokines and determined that at a dose of 50 pg/ml their rank order of activity was TGF-beta 1 > TNF-alpha > IL-1 > IL-6, with all but IL-6 having significant effects. The ability of supernatants from activated bone marrow-derived cultured mast cells to promote fibroblast proliferation was partially diminished by absorption with neutralizing antibodies against either TNF-alpha or TGF-beta 1, and absorption of the supernatants with a combination of antibodies against TNF-alpha and TGF-beta 1 reduced their ability to induce fibroblast proliferation by approximately 50% (p < or = 0.001, n = 5). These findings show that IgE-dependent activation of mouse mast cells can result in the release of mediators that promote fibroblast proliferation in the absence of any other cell type and suggest that mast cell-derived TNF-alpha and TGF-beta 1 contribute substantially to this effect. They also suggest that these cytokines exert their effects through synergistic interactions with other mast cell mediators.

Animals↗

PubMed1995

Induction of intra-articular tumour necrosis factor during acute inflammatory responses in equine arthritis.

Synovial fluid (SF) was collected at 2, 12 and 26 h post racing from 5 Thoroughbred horses (6 joints) with degenerative joint disease. The effects of serial arthrocentesis on SF TNF alpha levels were controlled for by testing, in parallel, site- and time-matched samples from clinically normal horses (i.e. without arthritis). A significant induction in TNF alpha bioactivity was detected in SF from arthritic joints (compared to the control joints) over the 26 h following racing. After subtraction of values for the arthrocentesis control SF, TNF alpha and protein levels and WBC and mononuclear cell numbers each peaked at 12 h in the SF from the degenerative joints, although there were no statistically significant correlations between any of these parameters. The presence in the SF of TNF alpha, as well as immunoreactive IL-1 beta and IL-6, was confirmed through use of specific anti-human cytokine IgG antibodies in neutralisation and slot-blot radioimmunoassays. TNF beta was not detected in the SF by slot-blot radioimmunoassay. These results suggest that a significant increase in intra-articular TNF alpha occurs during acute inflammatory arthritis in horses. The lack of correlation between infiltrating inflammatory cells and SF TNF alpha levels further suggests that the source of TNF alpha may be resident cells of the joint, as opposed to infiltrating cells found within the joint fluids. SF from clinically normal and arthritic joints of racing and hospitalised horses were also screened for bioactive TNF alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Promotion of mouse fibroblast collagen gene expression by mast cells stimulated via the Fc epsilon RI. Role for mast cell-derived transforming growth factor beta and tumor necrosis factor alpha.

Chronic allergic diseases and other disorders associated with mast cell activation can also be associated with tissue fibrosis, but a direct link between mast cell mediator release and fibroblast collagen gene expression has not been established. Using in situ hybridization, we show that the elicitation of an IgE-dependent passive cutaneous anaphylaxis (PCA) reaction in mice results in a transient, but marked augmentation of steady state levels of type alpha-1 (I) collagen mRNA in the dermis. While peak levels of collagen mRNA expression in the skin are observed 16-24 h after mast cell activation, substantial numbers of dermal cells are strongly positive for collagen mRNA at 1 and 2 h after antigen challenge, before circulating inflammatory cells are recruited into the tissues. Furthermore, experiments in mast cell-reconstituted or genetically mast cell-deficient WBB6F1-W/Wv mice demonstrate that the increased expression of collagen mRNA at sites of PCA reactions is entirely mast cell dependent. In vitro studies show that the supernatants of mouse serosal mast cells activated via the Fc epsilon RI markedly increase type alpha-1 (I) collagen mRNA levels in mouse embryonic skin fibroblasts, and also upregulate collagen secretion by these cells. The ability of mast cell supernatants to induce increased steady state levels of collagen mRNA in mouse skin fibroblasts is markedly diminished by absorption with antibodies specific for either of two mast cell-derived cytokines, transforming growth factor beta (TGF-beta 1) or tumor necrosis factor alpha (TNF-alpha), and is eliminated entirely by absorption with antibodies against both cytokines. Taken together, these findings demonstrate that IgE-dependent mouse mast cell activation can induce a transient and marked increase in steady state levels of type alpha-1 (I) collagen mRNA in dermal fibroblasts and that mast cell-derived TGF-beta 1 and TNF-alpha importantly contribute to this effect.

Animals↗

PubMed1994

Inhibition of endogenous dopamine release in amphibian retina by L-2-amino-4-phosphonobutyric acid (L-AP4) and trans-2-aminocyclopentane-1,3-dicarboxylate (ACPD).

The metabotropic glutamate receptor agonists 2-amino-4-phosphonobutyric acid (AP4) and trans-2-aminocyclopentane-1,3-dicarboxylate (ACPD) blocked light-stimulated dopamine release from Xenopus laevis retina. ACPD suppressed release in darkness but AP4 did not. AP4 blocked release stimulated in darkness by picrotoxin, a GABA-A receptor antagonist. The data suggest that regulation of dopamine release in Xenopus retina involves subpopulations of metabotropic glutamate receptors.

Aminobutyrates↗

PubMed1993

Mast cell cytokines in allergy and inflammation.

Recent findings indicate that mast cells can influence biological responses through the production of cytokines and suggest that many allergic reactions and other biological processes may be regulated by a "mast cell-leukocyte cytokine cascade". This hypothesis proposes that certain biological responses are initiated by mast cell activation, resulting in the mast cell-dependent release of TNF-alpha and other cytokines which can promote the recruitment of eosinophils, neutrophils, and other effector cells. The recruited effectors then influence the progression of the response by providing additional sources of some cytokines which also can be elaborated by mast cells, as well as by producing other cytokines not known to be of mast cell origin.

Animals↗

PubMed1993

Human eosinophils can express the cytokines tumor necrosis factor-alpha and macrophage inflammatory protein-1 alpha.

By in situ hybridization, 44-100% of the blood eosinophils from five patients with hypereosinophilia and four normal subjects exhibited intense hybridization signals for TNF-alpha mRNA. TNF-alpha protein was detectable by immunohistochemistry in blood eosinophils of hypereosinophilic subjects, and purified blood eosinophils from three atopic donors exhibited cycloheximide-inhibitable spontaneous release of TNF-alpha in vitro. Many blood eosinophils (39-91%) from hypereosinophilic donors exhibited intense labeling for macrophage inflammatory protein-1 alpha (MIP-1 alpha) mRNA, whereas eosinophils of normal donors demonstrated only weak or undetectable hybridization signals for MIP-1 alpha mRNA. Most tissue eosinophils infiltrating nasal polyps were strongly positive for both TNF-alpha and MIP-1 alpha mRNA. By Northern blot analysis, highly enriched blood eosinophils from a patient with the idiopathic hypereosinophilic syndrome exhibited differential expression of TNF-alpha and MIP-1 alpha mRNA. These findings indicate that human eosinophils represent a potential source of TNF-alpha and MIP-1 alpha, that levels of expression of mRNA for both cytokines are high in the blood eosinophils of hypereosinophilic donors and in eosinophils infiltrating nasal polyps, that the eosinophils of normal subjects express higher levels of TNF-alpha than MIP-1 alpha mRNA, and that eosinophils purified from the blood of atopic donors can release TNF-alpha in vitro.

Cells, Cultured↗

PubMed1992

Evaluation of dexamethasone for reduction of postsurgical sequelae of third molar removal.

Sixty patients with bilaterally symmetrical impacted third molars participated in this double-blind, within-subject study to quantify the effects of 4 mg of dexamethasone on reducing postsurgical sequelae. Each patient's surgery was staged by mouth side and completed in two appointments 5 to 6 weeks apart. A preoperative dose of dexamethasone given intravenously was randomized to mouth side and surgical appointment; sterile water served as a control. Major areas assessed in this study were facial swelling, pain, and trismus. No difference in swelling and daily pain was noted. However, trismus and global pain were significantly affected by the steroid. Patients had a daily postsurgical increase in incisal opening of 4 to 6 mm over the control side during the examination period. Patients evaluated pain by choosing the least painful side. By a greater than 4:1 margin, patients chose the steroid side as the least painful side. No increase in the rate or type of complications was detected between control and steroid sides.

Adolescent↗

PubMed1992

Analyzing mast cell development and function using mice carrying mutations at W/c-kit or Sl/MGF (SCF) loci.

Mast cells have been implicated in a wide variety of biological responses, but identifying the nature and importance of the mast cell's specific contributions to these reactions has been difficult. W/Wv mice have mutations affecting the c-kit tyrosine kinase receptor which is encoded at the W locus and which is necessary for normal mast cell development. In W/Wv mice, the cells which ordinarily give rise to normal mast cell populations do not adequately respond to a major migration, survival, proliferation and maturation factor expressed in the microenvironments where mast cells ordinarily develop: the c-kit receptor ligand, SCF. As a result, W/Wv mice virtually lack tissue mast cells. However, adoptive transfer to W/Wv mice of immature mast cells derived in vitro from the bone marrow cells of the congenic normal (+/+) mice selectively repairs the mast cell deficiency of the W/Wv recipients. These "mast cell knock-in" mice can be used to analyze the expression of biological responses in tissues which differ only because they do or do not contain populations of mast cells. This approach permits identification and quantification of the specific contributions of the mast cell to biological responses expressed in the skin, gastrointestinal tract and other anatomical sites, and also greatly facilitates analysis of the mechanisms by which mast cells influence these responses.

Animals↗

PubMed1991

Eosinophils from patients with blood eosinophilia express transforming growth factor beta 1.

The infiltration of eosinophils into tissues during pathologic responses is often associated with extracellular matrix alterations such as fibrosis. Transforming growth factor-beta 1 (TGF-beta 1) is a well-characterized multifunctional cytokine known to exert potent effects on the extracellular matrix. In this report, we showed the production of TGF-beta 1 by human eosinophils from patients with blood eosinophilia. Northern blot analysis using RNA isolated from eosinophils purified from a patient with the idiopathic hypereosinophilic syndrome (HES) detected the 2.5-kb TGF-beta 1 transcript. In situ hybridization and immunohistochemistry of leukocytes from two patients with HES and two patients with blood eosinophilia localized TGF-beta 1 messenger RNA (mRNA) and protein to eosinophils. No other cell type contained TGF-beta 1 mRNA by in situ hybridization, whereas other leukocytes contained detectable TGF-beta 1 protein by immunohistochemistry. Eosinophils from four normal donors contained little or no detectable TGF-beta 1 protein by immunohistochemistry, whereas eosinophils from two of these four normal donors labeled weakly for TGF-beta 1 mRNA by in situ hybridization. These results show that eosinophils in the peripheral blood of patients with blood eosinophilia can express TGF-beta 1, but that eosinophils in the blood of normal donors contained little or no TGF-beta 1.

Adult↗

PubMed1991

Release of both preformed and newly synthesized tumor necrosis factor alpha (TNF-alpha)/cachectin by mouse mast cells stimulated via the Fc epsilon RI. A mechanism for the sustained action of mast cell-derived TNF-alpha during IgE-dependent biological responses.

Mast cell-associated mediators are generally classified into two groups: the preformed mediators, which are stored in the cells' cytoplasmic granules and are released upon exocytosis, and the newly synthesized mediators, which are not stored but are produced and secreted only after appropriate stimulation of the cell. We now report that tumor necrosis factor alpha (TNF-alpha)/cachectin represents a new type of mast cell-associated mediator, in that IgE-dependent mast cell activation results in the rapid release of preformed stores of the cytokine followed by the synthesis and sustained release of large quantities of newly formed TNF-alpha. We also demonstrate that challenge with specific antigen induces higher levels of TNF-alpha mRNA at skin sites sensitized with IgE in normal mice or mast cell-reconstituted genetically mast cell-deficient WBB6F1-W/W1' mice than at identically treated sites in WBB6F1-W/W1' mice that are devoid of mast cells. These findings identify mast cells as a biologically significant source of TNF-alpha/cachectin during IgE-dependent responses and define a mechanism whereby stimulation of mast cells via the FC epsilon RI can account for both the rapid and sustained release of this cytokine.

Animals↗

PubMed1991

Cytokine production by mast cells and basophils.

Mast cells and/or basophils have been implicated in the expression of a wide variety of biological responses, including immediate hypersensitivity reactions, host responses to parasites and neoplasms, angiogenesis, tissue remodeling, and immunologically non-specific inflammatory and fibrotic conditions. Recent findings suggest that an important mechanism by which mast cells influence such biological responses is through the production of a broad panel of multifunctional cytokines. In contrast, the extent to which basophils can produce cytokines is uncertain.

Animals↗

PubMed1991

Recruitment of neutrophils during IgE-dependent cutaneous late phase reactions in the mouse is mast cell-dependent. Partial inhibition of the reaction with antiserum against tumor necrosis factor-alpha.

Much of the clinically important pathology associated with IgE-dependent disorders is thought to reflect the actions of the blood-borne leukocytes recruited during these responses. To evaluate the extent to which mast cells are responsible for the leukocyte infiltration associated with IgE-dependent cutaneous reactions, we attempted to elicit these responses in normal mice, genetically mast cell-deficient W/Wv mice, and in W/Wv mice selectively repaired of their mast cell deficiency by the intradermal injection of cultured mast cells derived from the congenic normal (+/+) mice. We found that the tissue swelling associated with IgE-dependent passive cutaneous anaphylaxis reactions developed rapidly and diminished markedly from 2 to 4 h after antigen challenge, but remained detectable for at least 24 h after elicitation of the responses. Infiltration of leukocytes (predominantly neutrophils) also occurred at these sites, but reached maximal levels 6-12 h after antigen challenge, persisted at high levels for 24 h, and largely waned by 48 h. Virtually all of the tissue swelling and leukocyte infiltration associated with IgE-dependent cutaneous reactions was mast cell dependent. Intradermal injection of 40 U of recombinant murine TNF-alpha (rmTNF-alpha) elicited neutrophil infiltration similar in magnitude and kinetics to that observed after IgE-dependent mast cell degranulation. A rabbit anti-rmTNF-alpha (R anti-rmTNF-alpha) antiserum, which was able to inhibit 84% of the neutrophil infiltration observed after i.d. injection of rmTNF-alpha, inhibited IgE-, and mast cell-dependent leukocyte infiltration by 47 +/- 7% in three separate experiments. These findings indicate that TNF-alpha contributes to mast cell-dependent recruitment of leukocytes during IgE-dependent cutaneous late phase reactions, but suggest that other mast cell-associated mediators probably also contribute to this response.

Animals↗