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T Cavallo

Publications and source records attributed to T Cavallo.

At least 55 records · Page 3Linked to original sources
PubMed1986

IgA-associated glomerulonephritides: a study with monoclonal antibodies.

Thirty-six renal biopsies from patients with various glomerulonephritides which exhibited prominent IgA deposits were studied by indirect immunofluorescence technique utilizing monoclonal antibodies specific for alpha chain (IgA), IgA1 and IgA2 subclasses, secretory IgA, and secretory component. The ability of the IgA deposits to bind free secretory component in vitro was examined in five biopsies of IgA nephropathy of Berger and in five biopsies of lupus nephritis. All the biopsies revealed IgA1 deposits. Associated IgA2 was found in lupus nephritides and hepatic glomerulopathy. Secretory IgA and free secretory component were not detected in any biopsy. In situ free secretory component binding was demonstrated in IgA nephropathy of Berger but not in lupus nephritides. These results indicate that polymeric IgA1 molecules are the chief nephritogenic antibodies in IgA nephropathy of Berger, that there is a high frequency of association of IgA1 and IgA2 in lupus nephritides and, perhaps, hepatic glomerulopathy, and that secretory IgA does not appear to play a role in IgA-associated glomerulonephritis.

Antibodies, Monoclonal↗
PubMed1986

Cutaneous secondary syphilis: preliminary immunohistopathologic support for a role for immune complexes in lesion pathogenesis.

A circulating immune complex-mediated pathogenesis for lesions of secondary syphilis has been postulated. Textbook descriptions of a lymphoplasmacytic histopathologic picture have contradicted a role for circulating immune complexes in lesion pathogenesis. Four patients with early cutaneous lesions of secondary syphilis were studied. All four patients had serum Raji cell and/or Clq binding assay evidence for circulating immune complexes. Three patients showed a neutrophilic vascular reaction on histologic study of early lesions. The patients studied had immunofluorescence microscopic evidence of immunoreactant deposition in dermal blood vessels (4 hours) and/or a neutrophilic vascular reaction (24 hours) after intradermal histamine injection. Dieterle staining of lesional tissue from all patients showed the presence of treponemal organisms in dermal blood vessels. This new preliminary evidence adds some support to a circulating immune complex-mediated pathogenesis of cutaneous lesions in human secondary syphilis.

Adult↗
PubMed1986

Primary idiopathic cutaneous pustular vasculitis.

Pustular cutaneous vasculitis results from a heterogeneous group of disorders characterized by pustules on purpuric bases. Although the cause of this group of conditions is diverse, the histopathologic picture of the lesions is the same, showing a Sweet's-like or leukocytoclastic vasculitis. These distinctive lesions may occur in patients with Behçet's syndrome, bowel-associated dermatosis-arthritis syndrome, or chronic gonococcemia. We describe, for the first time, a patient with primary idiopathic cutaneous pustular vasculitis. This patient had evidence of both circulating immune complexes and serum enhancement of neutrophil migration. Extensive evaluation failed to reveal any underlying systemic disease. A classification of the pustular vasculitides is proposed.

Adolescent↗
PubMed1986

Role of circulating immune complexes in human secondary syphilis.

Studies in animal models and in the glomerulonephritis of human secondary syphilis and results from in vitro assays have suggested a role for circulating immune complexes (CICs) in human secondary syphilis. Nine adult subjects with early secondary syphilis were studied. All patients tested had CICs on C1q-binding or Raji cell assays. Proteins previously described as Treponema pallidum-specific antigens were detected by radioimmunoblot techniques in CICs from all five subjects tested. Biopsy of early cutaneous lesions revealed immunoreactants (IgG, C3, and/or C1q) in three of nine subjects and treponemal antigen in six of eight subjects tested. Histamine was injected intradermally as a trap for CICs, and biopsy of these injection sites revealed immunoreactants in four of nine subjects and treponemal antigen in five of eight subjects tested. A neutrophilic vascular reaction consistent with CIC-mediated vessel damage was seen in three of nine lesions and six of nine histamine injection sites. Normal controls did not show these changes.

Antigen-Antibody Complex↗
PubMed1986

Human cytomegalovirus: development and progression of nuclear inclusions by primary clinical isolates and laboratory-adapted strains.

The morphogenesis of cytomegalovirus (CMV) nuclear inclusions (NIs) was investigated using unadapted clinical isolates and adapted laboratory strains. Both adapted and unadapted strains of CMVs induced NIs whose morphologic appearance was similar in human fibroblastic cells. Early NIs appeared as ring-like structures composed of dense granular and fibrillar material, while late NIs appeared to consist of multiple electron-lucent areas containing coarse granules and bounded by electron-dense fibrillar material (cellulae). Capsids and nucleocapsids were associated primarily with the electron-dense fibrillar material; however, developing nucleocapsids were most often observed at the interface of the electron-dense and -lucent areas. Although there was some variation in the rate of development and maturation of the NIs with the intensity of infection, all CMVs examined produced late NIs with similar organizational patterns consisting of cellulae. Substitution of human fibroblastic cells derived from various tissues as cellular substrate did not appreciably affect the results. Thus, the unique organization of the CMV late NI, consisting of multiple cellulae, appears to be an intrinsic feature of CMV replication since it seems to be independent of the extent of laboratory adaptation, the virus strain, the intensity of infection, or the cell type.

Cell Nucleus↗
PubMed1986

Clonality of the spontaneous immune response to DNA in murine lupus.

To probe the mechanism of spontaneous formation of anti-DNA antibodies, we studied the isotype distribution of anti-DNA antibodies in the plasma of NZB/W mice with incipient, chronic, and drug-attenuated nephritis. The concentration of anti-DNA antibodies in plasma did not discriminate between the various groups of mice, and the anti-DNA activity in renal eluates was very low and did not reflect the course of nephritis. Progression of incipient to chronic nephritis was associated with increase, and drug attenuation of nephritis with decrease, in plasma concentration of all isotypes tested. Anti-DNA antibodies were detected in all classes (IgG, IgM) of antibodies studied and the anti-DNA antibodies were found to be unrestricted with respect to IgG isotypes and within a given (IgG2a) isotype. The data indicate that the spontaneous immune response to DNA in NZB/W mice reflects activation of several autoreactive clones and that, overall, anti-DNA activity in the plasma or renal eluate is a poor predictor of extent of renal disease.

Animals↗
PubMed1986

Mechanism-oriented assessment of isotretinoin in chronic or subacute cutaneous lupus erythematosus.

Eight of ten patients with chronic or subacute cutaneous lupus erythematosus completed 16 weeks of oral isotretinoin therapy (80 mg/day). All eight patients noted an excellent clinical response without significant side effects. (Two patients did not return to initial two-week follow-up.) Peripheral blood B- and T-cell counts were unaffected by therapy. Therapy was associated with resolution of routine histopathologic abnormalities, conversion of abnormal lesional direct immunofluorescence microscopy to normal, normalization of the epidermis on electron microscopy, and reduction of all T cells near the dermoepidermal junction without change in ratio of T-helper/inducer cells to T-suppressor/cytotoxic cells. Isotretinoin is a clinically effective short-term therapy for chronic or possibly for subacute cutaneous lupus erythematosus. The primary mechanism of action remains unestablished.

Administration, Oral↗
PubMed1986

Thalidomide effects in Behçet's syndrome and pustular vasculitis.

Pustular vasculitis is a new disease concept that links cutaneous, and possibly systemic, aspects of Behçet's, bowel bypass, bowel-associated dermatosis-arthritis, and disseminated gonorrhea syndromes. The pathomechanism of pustular vasculitic lesion generation may relate to circulating immune complex (CIC)-mediated vessel damage and serum enhancement of neutrophil migration. Thalidomide, an oral pharmaceutical available on strict protocol, has therapeutic effects based on proposed modulation of CIC- and neutrophil-mediated cytotoxicity. Thalidomide therapy was started for four patients with significant morbidity from Behçet's syndrome and for one patient with bowel-associated dermatosis-arthritis syndrome. Clinical benefit was dramatic in all patients who completed sequential four-week "on" and "off" thalidomide therapeutic cycles. In three of four patients, in vivo testing for CIC after histamine injection immunopathology converted from positive (immunoreactant deposition in dermal vasculature [four hours after histamine] and CIC-mediated vasculitis [24 hours after histamine]) to negative during therapy. No effects were noted on neutrophil migration or on the LFA-1/Mac-1/p150,95 family of glycoproteins associated with neutrophil adherence as assessed qualitatively by tritium labelling of neutrophil cell surfaces. In this small patient group, thalidomide was a clinically effective, safe (with rigid monitoring) therapy whose mechanism of action may relate more to inhibitory effects on CIC-induced vasculitis than to effects on neutrophil-mediated cytotoxicity.

Antigen-Antibody Complex↗
PubMed1985

Complex aphthosis: a forme fruste of Behçet's syndrome?

The evaluation of the rare patient who presents with oral and genital aphthae or almost constant, multiple (greater than 3) oral aphthae, but no systemic signs or symptoms (i.e., complex aphthosis), is difficult because no laboratory test is available to exclude Behçet's syndrome. Six patients with complex aphthosis were evaluated. In addition, patients with simple aphthosis, those with seronegative arthritis, and normal controls were assessed for circulating immune complexes (CIC) by in vitro and in vivo assays and for neutrophil migration by subagarose methods, since these tests have given significant results in patients with Behçet's syndrome. Patient 1, with complex aphthosis, had Raji cell evidence for CIC (51.2 mg aggregated human gamma globulin Eq/ml), C1q, and C3 in dermal blood vessels 4 hours post intradermal histamine injection and had a Sweet's syndrome-like vasculitis 24 hours post histamine injection. In addition, her serum enhanced the migration of patient neutrophils (3.6 +/- 0.6 to 4.6 +/- 0.5; N = 6, p less than or equal to 0.01). All other test and control patients had negative or normal CIC and neutrophil migration determinations. Sixteen-month clinical follow-up has confirmed that Patient 1, but not Patients 2 to 6, has developed overt manifestations of Behçet's syndrome.

Adult↗
PubMed1985

Behçet's syndrome. Immunopathologic and histopathologic assessment of pathergy lesions is useful in diagnosis and follow-up.

Behçet's syndrome is a complex multisystem disease that, due to the absence of a pathognomonic laboratory test, must be diagnosed using clinical criteria. Clinical pathergy testing, the induction of a sterile pustule 24 hours after cutaneous trauma, has been proposed as a useful adjunct to diagnosis. We have expanded this concept by showing the usefulness of examining pathergy lesions by routine and immunofluorescence microscopy in the diagnosis of nine patients with Behçet's syndrome. Furthermore, histopathologic pathergy assessments correlated with clinical disease activity and/or response to experimental oral thalidomide therapy in five of six patients with Behçet's syndrome who were retested.

Adult↗
PubMed1985

Pathogenic role of anti-DNA antibodies in murine lupus nephritis.

We studied the relative role of anti-DNA antibodies in pathogenesis of murine lupus nephritis, and we used, as index of their contribution, the association between attenuation, or progression, of renal disease and decrease or increase in concentration of anti-DNA antibodies in the plasma and renal eluate of NZB/W mice. The concentration of anti-DNA antibodies in plasma did not discriminate mice with incipient or drug attenuated nephritis, who had normal renal function, from mice with progressive nephritis, who developed renal failure. Although the quantity of IgG eluted from kidneys reflected the extent of renal disease (mice with progressive nephritis greater than mice with attenuated nephritis greater than mice with incipient nephritis), the anti-DNA activity of such antibodies was negligible. The low anti-DNA activity could not be attributed to either excess DNA or DNAase in renal eluates. In fact, the eluates contained a factor that inhibited the interaction between anti-DNA antibody and DNA. The results indicate that immune complex systems other than, or in addition to, DNA-anti-DNA are likely to play a role in the pathogenesis of murine lupus nephritis.

Animals↗
PubMed1985

Influence of avidity of circulating anti-DNA antibodies on murine lupus nephritis.

We determined the avidity of antiDNA antibodies in plasma of NZB/W mice when nephritis became apparent, when such mice developed chronic glomerulonephritis, and in mice whose nephritis was arrested, or attenuated, by immunosuppression. Antibody avidity was estimated by the rate of dissociation of 125IDNA-antiDNA complexes when excess unlabelled DNA was added to the plasma. In all groups of mice studied, the relative contributions of high and low avidity antiDNA antibodies were comparable and, overall, high avidity antibodies predominated. The results indicate that the avidity of circulating antiDNA antibodies did not reflect the extent and type of glomerular involvement, and was not predictive of clinical course.

Animals↗
PubMed1985

Association of glycoprotein gp70 with progression or attenuation of murine lupus nephritis.

We studied the relative role of gp70-antigp70 complexes in the pathogenesis of murine lupus nephritis, and we used as an index of its contribution, the association between attenuation, or progression, of renal disease and decrease or increase in concentration of gp70 complexes and IgG in the plasma and renal eluate of NZB/W mice. The arrest or attenuation of nephritis, by immunosuppression, was associated with decreased concentrations in the plasma and renal eluates of IgG and gp70 complexes, and the relative concentration of these reagents in the eluates better reflected the extent of renal disease than did their concentration in the plasma. Neither the relative concentration of Clq-reactive materials, nor the quantity of antiDNA antibodies in the plasma, distinguished the mice whose nephritis was arrested by immunosuppression from those with terminal renal failure. The findings further support that the gp70-antigp70 system plays an important role in the pathogenesis of murine lupus nephritis.

Animals↗
PubMed1984

Bowel-associated dermatosis-arthritis syndrome. Immune complex-mediated vessel damage and increased neutrophil migration.

In a recent report we described a syndrome, identical to bowel-bypass syndrome, that occurred in four patients who had not had bypass surgery. Herein, circulating immune complexes (CICs) and neutrophil migration are evaluated in three of those four patients to test the hypothesis that the cutaneous lesions might have resulted from interaction between immune complex-mediated vessel damage and increased neutrophil migration. In vitro assays indicated that CICs were present in one of two patients and "histamine trap" test evidence for CICs was present in both patients tested. Although serum from the three patients appeared to increase neutrophil movement, statistically significant increases were not observed when data were pooled in this small study group. Preliminary results suggest that immune complex-mediated vessel damage, followed by extensive accumulation of neutrophils, may cause the pustular vasculitis in the bowel-associated dermatosis-arthritis syndrome.

Adult↗
PubMed1984

Behçet's syndrome: immune regulation, circulating immune complexes, neutrophil migration, and colchicine therapy.

Immune regulatory dysfunction, circulating immune complexes (CIC), and polymorphonuclear (PMN) cell migration were investigated in patients with Behçet's syndrome. Six patients meeting rigorous clinical criteria were evaluated. Only one patient showed evidence of immune regulatory dysfunction (increased T4/T8 ratio). Although C1q binding and Raji cell assays for CIC yielded positive results in only one of five patients, all five patients had in vivo "histamine trap test" evidence of CIC (all controls had normal results). Sera from all Behçet's syndrome patients increased migration of neutrophils to zymosan-activated serum. Colchicine therapy abolished the enhancing effect of the patient's sera on movement of PMN cells from patients and controls. An immune complex-mediated injury that is followed by an excessive accumulation of PMN cells may lead to the cutaneous lesions and other lesions in Behçet's syndrome. Further evaluation of colchicine therapy is warranted on the basis of these studies.

Adult↗
PubMed1984

Hyporeninemic hypoaldosteronism in a patient with multiple myeloma.

A patient with progressive renal failure due to multiple myeloma presented with a mixed acid-base disorder (non-anion gap acidosis and respiratory alkalosis) with persistent severe hyperkalemia. Studies revealed an intact ability to lower urine pH during acid loading, markedly decreased plasma renin and aldosterone concentrations despite volume depletion, and an inappropriately low fractional excretion of potassium. Renal biopsy demonstrated plasma cell infiltration of the renal interstitium and typical proteinaceous intratubular casts. Both proximal and distal renal tubular acidification defects have been described previously in patients with multiple myeloma, but this is the first report of hyporeninemic hypoaldosteronism, hyperkalemia, and hyperchloremic metabolic acidosis in association with renal involvement in multiple myeloma.

Acidosis↗