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PubMed2002

Development of inflammation in proteoglycan-induced arthritis is dependent on Fc gamma R regulation of the cytokine/chemokine environment.

FcgammaRs are specialized cell surface receptors that coordinately regulate immune responses. Although FcgammaR expression is a prerequisite for the development of several immune complex-mediated diseases, the mechanism responsible for FcgammaR-dependent regulation in autoimmunity remains unclear. Therefore, we assessed FcgammaR-dependent regulation of inflammation in proteoglycan-induced arthritis (PGIA) using FcgammaR(-/-) mice. FcgammaRIIb(-/-) mice developed arthritis at an earlier time point and with a greater severity than wild-type (WT) mice. In gamma-chain(-/-) (FcgammaRI(-/-) and FcgammaRIII(-/-)) mice, no clinical or histological evidence of inflammation was observed. Exacerbation of arthritis in FcgammaRIIb(-/-) mice correlated with enhanced PG-specific Ab production, but did not significantly affect PG-specific T cell priming. In gamma-chain(-/-) mice, the absence of arthritis did not correlate with serum Ab responses, as PG-specific Ab production was normal. Although PG-specific T cell proliferation was diminished, spleen cells from gamma-chain(-/-) mice successfully adoptively transferred arthritis into SCID mice. Our studies indicated that the mechanism responsible for FcgammaR regulation of PGIA development was at the level of inflammatory cytokine and beta-chemokine expression within the joint. FcgammaRIIb regulated the development of PGIA by controlling the initiation of cytokine and chemokine expression within the joint before the onset of arthritis, whereas the expression of FcgammaRI and or FcgammaRIII controlled cytokine and chemokine expression late in the development of PGIA during the onset of disease. These results suggest that FcgammaRs are critical for the development of inflammation during PGIA, possibly by maintaining or enhancing inflammatory cytokine and beta-chemokine production.

Adult↗
PubMed2006

4-Fluoroproline derivative peptides: effect on PPII conformation and SH3 affinity.

Eukaryotic signal transduction involves the assembly of transient protein-protein complexes mediated by modular interaction domains. Specific Pro-rich sequences with the consensus core motif PxxP adopt the PPII helix conformation upon binding to SH3 domains. For short Pro-rich peptides, little or no ordered secondary structure is usually observed before binding interactions. The association of a Pro-rich peptide with the SH3 domain involves unfavorable binding entropy due to the loss of rotational freedom on forming the PPII helix. With the aim of stabilizing the PPII helix conformation in the Pro-rich HPK1 decapeptide PPPLPPKPKF (P2), a series of P2 analogues was prepared, in which specific Pro positions were alternatively occupied by 4(S)- or 4(R)-4-fluoro-L-proline. The interactions of these peptides with the SH3 domain of the HPK1-binding partner HS1 were quantitatively analyzed by the NILIA-CD approach. A CD thermal analysis of the P2 analogues was performed to assess their propensity to adopt the PPII helix conformation. Contrary to our expectations, the K(d) values of the analogues were lower than that of the parent peptide P2. These results clearly show that the induction of a stable PPII helix conformation in short Pro-rich peptides is not sufficient to increase their affinity toward the SH3 domain and that the effect of 4-fluoroproline strongly depends on the position of this residue in the sequence and the chirality of the substituent in the pyrrolidine ring.

Adaptor Proteins, Signal Transducing↗
PubMed2006

The crystal structure of mouse Nup35 reveals atypical RNP motifs and novel homodimerization of the RRM domain.

The nuclear pore complex mediates the transport of macromolecules across the nuclear envelope (NE). The vertebrate nuclear pore protein Nup35, the ortholog of Saccharomyces cerevisiae Nup53p, is suggested to interact with the NE membrane and to be required for nuclear morphology. The highly conserved region between vertebrate Nup35 and yeast Nup53p is predicted to contain an RNA-recognition motif (RRM) domain. Due to its low level of sequence homology with other RRM domains, the RNP1 and RNP2 motifs have not been identified in its primary structure. In the present study, we solved the crystal structure of the RRM domain of mouse Nup35 at 2.7 A resolution. The Nup35 RRM domain monomer adopts the characteristic betaalphabetabetaalphabeta topology, as in other reported RRM domains. The structure allowed us to locate the atypical RNP1 and RNP2 motifs. Among the RNP motif residues, those on the beta-sheet surface are different from those of the canonical RRM domains, while those buried in the hydrophobic core are highly conserved. The RRM domain forms a homodimer in the crystal, in accordance with analytical ultracentrifugation experiments. The beta-sheet surface of the RRM domain, with its atypical RNP motifs, contributes to homodimerization mainly by hydrophobic interactions: the side-chain of Met236 in the beta4 strand of one Nup35 molecule is sandwiched by the aromatic side-chains of Phe178 in the beta1 strand and Trp209 in the beta3 strand of the other Nup35 molecule in the dimer. This structure reveals a new homodimerization mode of the RRM domain.

Amino Acid Motifs↗
PubMed1981

Prevention of glomerulonephritis and prolonged survival in New Zealand Black/New Zealand White F1 hybrid mice fed an essential fatty acid-deficient diet.

Female B/W mice spontaneously develop an autoimmune disease that is similar to systemic lupus erythematosus. Antibodies to doublestranded DNA (dsDNA) and antinuclear antibodies develop in aging animals; death from immune complex-mediated glomerulonephritis occurs from 8 to 12 mo of age. It has been reported that prostaglandin (PG)E(1) treatment of such mice prolongs survival. In the present study, four groups of female B/W mice were studied beginning at 6-11 wk of age on the following regimens: (a) a synthetic diet that contained 20% safflower oil, (b) a standard laboratory chow diet, (c) a standard diet together with injections of PGE(1), and (d) an essential fatty acid-deficient synthetic diet that contained 20% coconut oil. All animals were tested monthly for antinuclear antibodies and anti-dsDNA. Kidney tissue was obtained for light and immunofluorescence microscopy when animals were dying. All disease manifestations were altered strikingly in the essential fatty acid (EFA)-deficient animals. Intermediate benefit was seen in PGE(1)-treated animals. 7% of the control animals and 18% of safflower oil-fed animals survived to 10 mo. In contrast, the PGE(1)-treated and EFA-deficient mice had a similar survival rate (78-88%). At age 16 mo, 78% of EFA-deficient mice and 45% of PGE(1)-treated mice were alive. 25% of the PGE(1)-treated and 55% of the EFA-deficient animals survived to 20 mo. Serum anti-dsDNA appeared at age 5 mo in safflower oil-fed and control animals, but not until 9 and 12 mo for PGE(1)-treated and EFA-deficient animals, respectively. All kidneys from 7- to 9-mo-old safflower oil-fed and control animals and the majority of kidneys from PGE(1)-treated animals were abnormal by light and immunofluorescence microscopy. Kidneys from EFA-deficient animals were essentially normal at 10 mo. At 13 mo, all PGE(1)-treated animals examined had significant kidney involvement, whereas none of the EFA-deficient animals had glomerulonephritis. These findings demonstrate that an EFA-deficient diet has a beneficial effect on murine lupus erythematosus.

Age Factors↗
PubMed1986

Arthritis in children with bacterial meningitis.

Forty-eight patients with arthritis and meningitis were identified by hospital chart review among 2,089 cases of bacterial meningitis treated between 1969 and 1984. The etiologic agents were Haemophilus influenzae in 38 cases (79%), Neisseria meningitidis in nine cases (19%), and Staphylococcus aureus in one case (2%). Thirteen patients had more than one joint affected: two affected joints, ten patients; three affected joints, two patients; and four affected joints, one patient. The elbow (34%) and knee (29%) were most frequently affected. Joint-fluid aspirations were done in 44 patients; 22 cases (50%) had bacteria or bacterial antigen identified in joint fluid by culture, Gram's stain, or counter-immunoelectrophoresis: H influenzae (20 cases), N meningitidis (one case), and S aureus (one case). Of the 48 patients, 14 patients were noted to have arthritis at the time of diagnosis of meningitis, 16 patients on the first to sixth day, and 17 patients on the seventh day of treatment or later; one patient developed arthritis 12 days after treatment of H influenzae meningitis had been stopped. Fourteen cases with a culture-proved bacterial etiology of the arthritis developed arthritis within four days of treatment; the exception was a patient who developed arthritis after treatment of meningitis was stopped. Of the 21 patients with culture-negative joint fluid and who developed arthritis later in the course of treatment, 19 patients were considered to have possible immune complex arthritis. Management consisted of antibiotic therapy in all patients, open incision and drainage in 17 patients (36%), and multiple aspirations in 12 patients (25%). Of the remaining 19 patients, 15 patients had a single arthrocentesis performed and four patients had no aspiration. Early-onset arthritis appeared to be related to bacteremia whereas late-onset arthritis may be immune complex mediated.

Adolescent↗
PubMed1991

Lower extremity arterial disease in systemic lupus erythematosus.

Lupus vasculitis primarily affects microvascular circulation, and large-vessel thrombosis is a rare complication of this disease. Large-vessel occlusive disease in systemic lupus erythematosus is most likely related to hypercoagulability in addition to immune complex-mediated endothelial damage. We describe the 11th and 12th patients reported to have systemic lupus erythematosus and macrovascular occlusive disease of the lower extremities. Our experience and a review of the literature suggest that, while aortoiliac disease is amenable to bypass or endarterectomy, infrainguinal disease is rarely correctable surgically, and amputation becomes necessary in most of these patients.

Adolescent↗
PubMed2000

Effects of hypoxia on granulocytic-monocytic progenitors in rats. Role of bone marrow stroma.

Hemorrhagic shock leads to hypoxia and is associated with bone marrow (BM) failure. Hemorrhagic shock is also a predisposing factor in immune dysregulation. Since the BM is the major organ of immune cells in the adult, its failure following hemorrhagic shock may explain the increased susceptibility to infection. The in vitro evidence indicates that hypoxia mediates altered functions in BM stroma. Since similar hematopoietic alterations are reported in hypoxia and hemorrhagic shock, hypoxia alone could be a representative model to study BM responses during hemorrhagic shock. In this study, we use an animal model to dissect the hematopoietic effects of hypoxia. We subjected rats to hypoxia, and at days 1 and 5 post-hypoxia we determined the numbers of granulocytic-monocytic progenitors (CFU-GM) in the BM. We found significant increase (P < 0.05) in CFU-GM at day 1 and a downward trend by day 5. Enhanced BM cellularity could not explain the increase in CFU-GM by day 1. BM stromal cells mediated most of the stimulatory effects by hypoxia. CFU-GM was inversely proportional to bioactive TGF-beta and directly proportional to IL-1. Compared to normoxic rats, IL-6 production was suppressed in BM cells from hypoxic rats. The results show that hypoxia alone initiate a stimulatory response in CFU-GM progenitors. These effects are at least partially mediated through the BM stroma. In the absence of a second insult, CFU-GM reverts to baseline. The data also suggest that hypoxia mediates complex responses that include cytokine production. These results add to the current understanding of hematopoietic responses by hypoxia and adds to the mechanisms of immune dysfunctions following hemorrhagic shock.

Animals↗
PubMed1996

Adhesion molecules in human crescentic glomerulonephritis.

The expression of the intercellular adhesion molecule-1 (ICAM-1) and its ligand lymphocyte function associated antigen-1 (LFA-1 or alpha L), the vascular cell adhesion molecule-1 (VCAM-1), endothelial leukocyte adhesion molecule-1 (ELAM-1), and the cellular receptors for extracellular matrix, alpha 1, alpha 2, alpha 3, alpha 5, alpha 6, alpha V, beta 1, and beta 3 integrin subunits, was studied in 28 patients with crescentic glomerulonephritis (GN) related to several mechanisms: four patients with anti-glomerular basement membrane antibodies or anti-GBM disease; 16 with immune complex mediated GN; and eight with pauci-immune GN, associated with vasculitis in four cases. A three-step immunoperoxidase technique was used on sections obtained from frozen renal biopsies. At the initial stage of evolution of the lesions, all the cells of the crescents expressed the beta 1, beta 3, alpha 1, alpha 3, and alpha V subunits of integrins, ICAM-1, and VCAM-1, and some cells expressed the alpha 2, alpha 5, alpha 6, and alpha L subunits of integrins along the plasma membrane. At a later stage, when the crescents were fibrocellular, alpha 3 and alpha 1 subunit expression was polarized, localized mainly in front of the extracellular matrix. In fibrotic crescents, the alpha 2, alpha 5, alpha 6, and alpha L chains were no longer detected, and VCAM-1 and ICAM-1 expression was decreased. VCAM-1 and ELAM-1 appeared on endothelial cells of peritubular capillaries in relation to the appearance of infiltrating inflammatory cells. The results of this study show that several adhesion molecules were expressed on cells forming crescents and were modified during crescent evolution; that these molecules were up-regulated on endothelial cells in relation to the severity of the inflammatory response; and that whatever the mechanism of the glomerulonephritis, adhesion molecule expression was identical. It can be postulated that adhesion molecules play a role in crescentic glomerulonephritis. Better knowledge of these molecules in human glomerulonephritis may open the way to a new therapeutic approach.

Cell Adhesion Molecules↗
PubMed1999

Differential expression of collagen type IV alpha-chains in the tubulointerstitial compartment in experimental chronic serum sickness nephritis.

The expression of collagen type IV chains in the renal tubulointerstitium was investigated during the development of chronic serum sickness (CSS) in rats, a model for immune complex-mediated renal disease. Immunohistochemical studies showed increased expression of alpha4(IV) collagen early during disease development, followed by an increase in alpha1(IV) through alpha3(IV) collagen subchain expression, especially in the tubular basement membrane. Dot-blot and in situ hybridization analysis showed a transient increase in steady-state mRNA levels for all collagen IV subchains during the development of CSS, which was most abundant for alpha1(IV), alpha2(IV), and alpha4(IV). Statistical correlations were found between the mRNA levels of alpha1(IV) and alpha2(IV) collagen and between alpha3(IV) and alpha4(IV), in line with the results of others which showed that these chains are co-distributed as heterotrimer collagen type IV molecules. However, additional correlations were found between the mRNA levels coding for alpha1(IV) and alpha3(IV) collagen, and between alpha1(IV) and alpha4(IV) mRNAs in the course of CSS. These abnormal correlations support the hypothesis that changes occur in the co-expression of the collagen IV subchains during the development of CSS. In addition, a strong correlation was found between the presence in the tubulointerstitium of alpha1(IV) and alpha2(IV) collagen chains, on the one hand, and the tubulointerstitial influx of R73+ and ED1+ cells, on the other, suggesting the involvement of inflammatory cells in the observed alterations in matrix production. Changes in the relative abundance of collagen IV chains in disease states may perturb the collagen IV network in the tubulointerstitial compartment and thereby play a role in the development of renal failure.

Animals↗
PubMed1997

The sequence of a nearly unclonable 22.8 kb segment on the left arm chromosome VII from Saccharomyces cerevisiae reveals ARO2, RPL9A, TIP1, MRF1 genes and six new open reading frames.

The nucleotide sequence of 22,803 bp on the left arm of chromosome VII was determined by polymerase chain reaction-based approaches to compensate for the unstable character of cosmid clones from this region of the chromosome. The coding density of the sequence is particularly high (more than 83%). Twelve open reading frames (ORFs) longer than 300 bp were found, two of which (at the left side) have been described previously (James et al., 1995) after sequencing of an overlapping cosmid. Four other ORFs correspond to published sequences of the known genes ARO2, RPL9A, TIP1 and MRF1. ARO2 codes for chorismate synthetase. RPL9A for protein L9 of the large ribosomal subunit and MRF1 for a mitochondrial translation release factor. The TIP1 product interacts with Sec20p and is thus involved in transport from endoplasmic reticulum to Golgi. Five of the remaining ORFs have not been identified previously, while the sixth (YGL142c) has been partially sequenced as it lies 5' upstream of MRF1. These six ORFs are relatively large (between 933 and 3657 nucleotides). YGL146c, YGL142c, YGL140c and YGL139w have no significant homology to any protein sequence presently available in the public databases, but show two, nine, nine and eight putative transmembrane spans, respectively. YGL144c has a serine active site signature of lipases. YGL141w has limited homology to several human proteins, one of which mediates complex formation between papillomavirus E6 oncoprotein and tumor suppressor protein p53.

Arabidopsis Proteins↗
PubMed1999

M6P/IGFII-receptor complexes urokinase receptor and plasminogen for activation of transforming growth factor-beta1.

Transforming growth factor-beta1 (TGF-beta1) is a critical cytokine for cell proliferation and differentiation. It is secreted by many cells in a latent pro-form (LTGF-beta1) from which biologically active TGF-beta1 is released by an in vivo mechanism that is not known. Here we show that the mannose-6-phosphate/insulin-like growth factor II-receptor (M6P/IGFII-R), which binds LTGF-beta1, complexes with urokinase (plasminogen activator)-receptor (uPA-R) on the surface of human monocytes and directly binds plasminogen (Plg). Plasmin generated from Plg in the complex mediates release of TGF-beta1 when M6P/IGFII-R is associated with uPA-R. Thus, this interaction of M6P/IGFII-R and uPA-R suggests a potential mechanism for the generation of TGF-beta1 by cells.

Amino Acid Sequence↗
PubMedDate not supplied

Organic brain syndrome in rheumatoid arthritis following corticosteroid withdrawal.

Six patients with seropositive nodule-forming rheumatoid arthritis developed severe central nervous system manifestations consistent with a diagnosis of organic brain syndrome. Organic brain syndrome occurred while 5 of these patients were undergoing corticosteroid withdrawal after prolonged administration. Neuropsychiatric symptoms rapidly cleared, responding to reinstitution of oral or parenteral corticosteroids in large doses in 4 patients, to increase in dosage in 1 patient, and to no drug therapy in the remaining 1. Marked reduction in rheumatoid factor in sera and demonstration of IgM deposits in the choroid plexus in 1 of the patients raised the possibility of immune complex-mediated central nervous system vasculitis.

Adrenal Cortex Hormones↗
PubMed1981

Native type II collagen--induced arthritis in the rat: the effect of complement depletion by cobra venom factor.

Antibodies to native bovine type II collagen may be important in initiating arthritis in rats immunized with this antigen. The cross-reactivity of these antibodies with native rat type II collagen was higher in rats that developed arthritis than in those that did not. Depletion of serum C3 levels by cobra venom factor delayed the onset of arthritis until C3 levels were returning to normal; therefore, complement may be involved in initiation of the arthritis, and this arthritis may be an example of an immune complex--mediated disease.

Animals↗
PubMed1982

Adult-onset Still's disease. Twenty-year followup and further studies of patients with active disease.

Eleven female patients with adult-onset Still's disease were followed for 7-36 years (mean 20.2 years) after the onset of their illness. Ten of these patients had a chronic course characterized by remissions and exacerbations of arthritis associated with fever and rash. Five patients had terminal interphalangeal involvement, and carpal ankylosis was demonstrated on x-ray film in 10. Two patients developed a widespread polyarthritis, and renal amyloidosis was diagnosed 10 years after disease onset in the most severely affected patient. In 4 patients studied during an exacerbation of the disease, circulating immune complexes were detected by the staphylococcal A binding assay, but not by the C1q binding assay. Synovial fluid analysis in 1 patient revealed a low C3 level and total hemolytic complement (CH50) together with immune complexes and IgG rheumatoid factor. Immune complexes were not identified in the characteristic Still's rash by immunofluorescence or electron microscopy, although mast cell degranulation, neutrophil lysis, and perivascular fibrin deposition were reminiscent of immune complex--mediated vascular injury. The clinical and laboratory features as well as the long-term course of adult- and juvenile-onset systemic Still's disease are similar, but further studies of genetic markers and immunopathology are required to establish a common pathophysiology.

Adult↗
PubMed1986

Estimation of the relative avidity of 19S IgM rheumatoid factor secreted by rheumatoid synovial cells for human IgG subclasses.

19S IgM rheumatoid factors (RF) may play an important role in sustaining inflammation in rheumatoid arthritis (RA). As yet, no unique antigenic specificity for RF in RA has been identified. Because the synovium is central to the pathogenic changes in RA, RF produced therein might be pathogenically more important than serum RF. Therefore, we examined the reactivity and relative avidity of 19S IgM-RF in serum and rheumatoid synovial cells (RSC) from 20 patients with seropositive RA. Reactivities were determined by competitive inhibition of serum RF hemolytic activity and RSC RF-plaque-forming cells (PFC) by added soluble antigen, i.e., monomeric human IgG subclasses. Estimation of relative avidities of RSC RF for human IgG subclasses was done by calculation of fractional RF expression in the RSC RF-PFC assay following inhibition by IgG subclasses. RSC RF had greatest reactivity with IgG3 and IgG1, some reactivity with IgG2, and the least reactivity with IgG4. Serum RF reacted most with IgG1 and IgG2, reacted some with IgG4, but reacted poorly with IgG3. The antigenic determinants with which RSC RF reacted were common to many IgG3 molecules. The highest relative avidity of RSC RF was for IgG3. These observations indicate a selective deficiency of serum RF compared with RSC RF and suggest an important pathogenic role for these qualitatively different RSC RF molecules for in situ RF immune complex-mediated inflammation in RA synovial tissue.

Animals↗
PubMed1986

Cryoglobulinemia in autoimmune rheumatic diseases. Evidence of circulating monoclonal cryoglobulins in patients with primary Sjögren's syndrome.

The incidence and nature of cryoglobulins, as well as their correlation with the clinical and serologic picture of Sjögren's syndrome (SS), were studied in the sera of 30 consecutive primary SS patients. Sera from 29 patients with systemic lupus erythematosus, 58 patients with rheumatoid arthritis, and 125 healthy blood donors were also studied. It was shown that one-third of the patients with SS had cryoglobulinemia. These cryoglobulins were mixed monoclonal IgM immunoglobulins, whereas those observed in systemic lupus erythematosus and rheumatoid arthritis patients were mixed polyclonal. The nature of the cryoglobulins was demonstrated using high-resolution electrophoresis combined with immunofixation. The presence of cryoglobulins in the sera of SS patients correlated with extraglandular disease and with antibodies to Ro (SS-A) and IgM rheumatoid factor. SS patients with cryoglobulins had lower serum C4 levels than did patients without cryoglobulins. These findings suggest that SS expresses, in addition to polyclonal B cell hyperreactivity, a monoclonal process in the absence of lymphoid neoplasia. Further, they show that the extraglandular manifestations of the syndrome may be due to an immune complex-mediated pathology.

Adult↗
PubMed1987

Evidence of immune deposits and of basement membrane alterations in dermal vessels of normal skin of patients with essential mixed cryoglobulinemia.

To gain insight into the pathogenic mechanisms of immune complex-mediated vasculitis, clinically normal skin specimens from the forearms of 12 patients with essential mixed cryoglobulinemia were investigated by light microscopy, immunofluorescence microscopy, and electron microscopy. Basement membrane alterations were documented in 9 patients. Eleven patients had deposits in vessel walls, but only in 1 was there evidence of inflammation. The same immunoglobulins of the cryoproteins could be demonstrated in the tissue deposits by immunofluorescence analysis and by immunoelectron microscopy. These findings suggest that, in essential mixed cryoglobulinemia, immune reactants in dermal vessels of normal skin are more common than is evidenced by clinical examination. Moreover, it seems that cryoglobulins, as such, are not sufficient to trigger an inflammatory process: Additional local or plasma factors are required. Deposits were absent in 7 patients with cryoglobulinemia that was associated with a primary disorder. This could be ascribed to the lower cryocrit levels documented in this group of patients, or to the shorter duration of their disease.

Adult↗
PubMed1994

Nomenclature of systemic vasculitides. Proposal of an international consensus conference.

The following are some of the conclusions and proposals made at the Chapel Hill Consensus Conference on the Nomenclature of Systemic Vasculitis. 1. Although not a prerequisite component of the definitions, patient age is recognized as a useful discriminator between Takayasu arteritis and giant cell (temporal) arteritis. 2. The name "polyarteritis nodosa," or alternatively, the name "classic polyarteritis nodosa," is restricted to disease in which there is arteritis in medium-sized and small arteries without involvement of smaller vessels. Therefore, patients with vasculitis affecting arterioles, venules, or capillaries, including glomerular capillaries (i.e., with glomerulonephritis), are excluded from this diagnostic category. 3. The name "Wegener's granulomatosis" is restricted to patients with granulomatous inflammation. Patients with exclusively nongranulomatous small vessel vasculitis involving the upper or lower respiratory tract (e.g., alveolar capillaritis) fall into the category of microscopic polyangiitis (microscopic polyarteritis). 4. The term "hypersensitivity vasculitis" is not used. Most patients who would have been given this diagnosis fall into the category of microscopic polyangiitis (microscopic polyarteritis) or cutaneous leukocytoclastic angiitis. 5. The name "microscopic polyangiitis," or alternatively, "microscopic polyarteritis," connotes pauci-immune (i.e., few or no immune deposits) necrotizing vasculitis affecting small vessels, with or without involvement of medium-sized arteries. Cryoglobulinemic vasculitis, Henoch-Schönlein purpura, and other forms of immune complex-mediated small vessel vasculitis must be ruled out to make this diagnosis. 6. The name "cutaneous leukocytoclastic angiitis" is restricted to vasculitis in the skin without involvement of vessels in any other organ. 7. Mucocutaneous lymph node syndrome must be present to make a diagnosis of Kawasaki disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Antineutrophil Cytoplasmic↗