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Immune Globulin (immune + globulin)
Kinds of Immune Globulin Selected AbstractsRecent advances in the management and prophylaxis of respiratory syncytial virus infectionACTA PAEDIATRICA, Issue 2001A Greenough Respiratory syncytial virus (RSV) infection is an important cause of morbidity, particularly in prematurely born infants who have had chronic lung disease. Current therapy is essentially supportive. Overall, the results of randomized trials do not support the use of bronchodilators, corticosteroids or Ribavirin. Nitric oxide and exogenous surfactant may improve the respiratory status of those infants who require ventilatory support. Nosocomial infection can be reduced by appropriate handwashing. There is no safe and effective vaccine for use in infants. Immunoprophylaxis reduces hospitalization and requirement for intensive care. Palivizumab, a humanized monoclonal antibody, is preferred to RSV immune globulin as the immunoprophylactic agent. Immunoprophylaxis should be reserved for infants at highest risk of severe respiratory syncytial virus infection, if this strategy is to be used most cost-effectively. [source] Hepatitis B immune globulin to prevent hepatitis B virus graft reinfection following liver transplantation: A concise reviewHEPATOLOGY, Issue 6 2000Daniel Shouval First page of article [source] Dermatomyositis presenting as panniculitisINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 2 2000Yen-Yu Chao MD A 44-year-old obese woman was transferred to our clinic with a diagnosis of panniculitis. Examination showed multiple, indurated, erythematous, painful nodules and plaques distributed on the shoulders, back, forechest, abdomen, buttock, and bilateral thighs. These skin lesions appeared 2 months previously, measured 5,8 cm, and were tender on palpation. No obvious inducing factor was traced. The lesions seemed unresponsive to treatment with nonsteroidal anti-inflammatory drugs (ibuprofen, 400 mg three times a day) as similar lesions appeared in subsequent visits. Progressive proximal muscle weakness was found 1 month later. She was then admitted via the emergency room because of extensive painful skin plaques and abdominal pain. Diffuse erythematous to violaceous swelling of the face, neck, and shoulder was noted at about the same time ( Fig. 1). A skin biopsy specimen from the nodular lesion showed poikilomatous epidermal changes ( Fig. 2), and marked mononuclear cell infiltration in the dermis and subcutaneous fat ( Fig. 3). Dermatomyositis was considered as the diffuse violaceous facial erythema could be a form of heliotrope eruption, but Gottron's papule was not found. At admission, serum creatinine phosphokinase (CPK) was mildly elevated (436 IU/L; normal range, 20,170 IU/L), but serum asparagine transaminase (AST) and lactate dehydrogenase (LDH) levels were within normal limits (36 IU/L; normal, 11,47 IU/L; and 108 IU/L; normal, 90,280 IU/L, respectively). Antinuclear antibody was 1 : 80 positive with an atypical speckled pattern. Muscle strength was weakest during the first 2 days, about grade 3 by the Medical Research Council (MRC) of Great Britain scale. Gower's sign was positive. An electromyogram showed myopathic changes and a nerve conduction velocity study was normal. Serum enzymes were elevated further on the third day: AST, 55 IU/L; CPK, 783 IU/L with 100% MM form. The diagnosis of dermatomyositis was established. As for the work-up result, anti-dsDNA antibody, anti-ENA antibody, and anti-Jo1 antibody were negative. Tumor marker screen (,-HCG, AFP, CEA, and CA-125), was negative, and rhinolaryngopharyngoscope examination and gynecologic sonography were normal. Figure 1. Diffuse erythematous swelling with subtle violaceous hue extending from the temporal area to the cheeks, neck, and shoulders. The crusted lip ulcers of herpes simplex were also noted Figure 2. Basketweave hyperkeratosis, mild acanthosis, subtle vacuolar degeneration of the basal cells, and melanin incontinence (hematoxylin and eosin, ×400) Figure 3. Heavy mononuclear cells infiltrated in the subcutaneous fat tissue (hematoxylin and eosin, ×100) Pancreatitis was initially suspected because of epigastric pain and tenderness, elevated serum lipase (382 U/L; normal, 23,200 U/L), and amylase (145 U/L; normal, 35,118 U/L). No evidence of pancreatitis could be found in abdominal sonography and abdominal computed tomography (CT), however. The epigastric pain and tenderness subsided soon after admission and the serum pancreatic enzyme level declined on the second day (amylase 69 U/L; lipase, 276 U/L). The patient was then diagnosed with dermatomyositis and treated with prednisolone (120 mg/day). CPK dropped dramatically from 3286 IU/L the day before treatment to 1197 IU/L 3 days after. Panniculitis lessened and the muscle power improved after 1 week of treatment. The disease activity fluctuated even with treatment with prednisolone and the patient often felt listless and weak. The muscle weakness sometimes deteriorated to affect the patient's mobility. Facial erythema and panniculitis-like lesions were found during the worse times. Methotrexate and azathioprine were then added (7.5 mg and 250 mg per week, respectively), but CPK was still mildly elevated (189 IU/L), and the patient still felt ill. Human immune globulin (5%, 500 mL per day, 5 days per month) intravenous infusion was initiated thereafter. There was a dramatic response. Full muscle strength was retained and CPK was within the normal range in the following 6 months with only immune globulin therapy. [source] Public health measures to control hepatitis B virus infection in the developing countries of the Asia,Pacific regionJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2000Ding-Shinn Chen Hepatitis B virus (HBV) infection is prevalent in the Asia,Pacific region and the disease burden caused by chronic HBV infection has been enormous. Although vaccination programmes have been implemented in the past decade, and there are extremely successful countries in the region, many countries still cannot afford a control program. These countries are often populous and highly endemic for HBV infection. To overcome this, aid from developed countries or private foundations should be actively sought. In the developing countries of this region, HBV infection in early childhood is the main cause of chronic HBV status, and thus universal vaccination of all infants is the best way to control HBV infection. Because of the expense and extra costs of screening pregnant women, the use of hepatitis B immune globulin may not be essential. To achieve the goal of universal infant vaccination, public education should be done in parallel with education of health professionals and control measures. The Asia,Pacific region has more people with chronic hepatitis B than any other part of the world, and control of HBV infection in this region will no doubt be the most important and challenging task to be taken in the beginning of the new millennium. [source] Evidence of partial unfolding of proteins at the ice/freeze-concentrate interface by infrared microscopyJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 9 2009J. Jeff Schwegman Abstract The goal of this research was to use infrared spectroscopy in combination with a freeze drying stage to gain a better understanding of the mechanism of loss of protein integrity due to the stresses associated with freezing. Infrared spectra were collected in triplicate for the interstitial space between ice crystals and through ice crystals in a partially frozen system. Spectra were collected for lactate dehydrogenase (LDH) and human immune globulin (IgG) both in the presence and absence of an added surfactant (polysorbate 80). Spectra collected in the interstitial space, distant from the surface of ice crystals, were very similar to spectra collected from the initial solution regardless of the presence of a surfactant. Spectra collected through ice crystals, without added surfactant, were significantly different than spectra collected from the initial solution. An increase in bands characteristic of intermolecular ,-sheet structures (main component of aggregates) were present in these spectra. The presence of surfactant in both protein formulations resulted in a decrease in intermolecular ,-sheet signals in spectra of the proteins on the ice crystal surface. Additionally, much of the native state structure of LDH initially lost on the surface of ice crystals returned when surfactant was added to the formulation prior to freezing. © 2009 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 98:3239,3246, 2009 [source] Prophylaxsis against recurrance of hepatitis B virus after liver transplantation: a retrospective analysis spanning 20 yearsLIVER INTERNATIONAL, Issue 1 2008Nevin Yilmaz Abstract Liver transplantation (LT) in patients with hepatitis B virus (HBV) infection is associated with a high rate of graft loss and poor survival, unless re-infection can be prevented. Human hepatitis B immune globulin (HBIG) has long been utilized to prevent re-infection. More recently, an anti-viral agent has been utilized along with HBIG. However, the regimens utilized have varied considerably among LT programmes and the optimal regimen has never been defined. We conducted a retrospective analysis of 41 patients who underwent LT for HBV at our centre since 1985 and received either HBIG with or without an anti-viral agent. The mean age of these patients was 46 years; 81% were male and 88% white. The mean and maximal follow-up were 5.9 and 15 years respectively. Eight out of 15 E-antigen-positive patients who received HBIG alone developed recurrence after a mean of 17 months. In contrast, none of 10 E-Ag-negative patients who received HBIG alone and none of the 10 E-antigen-positive patients who received both HBIG and either lamivudine or adefovir developed recurrence. As long as the anti-HB surface remained detectable, no absolute minimum serum level appeared to lead to recurrent HBV. We concluded that recurrence of HBV following LT can be prevented in E-antigen-positive patients with a combination of HBIG and an anti-viral agent. In contrast, recurrence can be prevented in E-antigen-negative patients with HBIG alone. Maintaining a serum anti-HB surface level above a minimum arbitrary titre of 200 pg/mL did not appear to be necessary for effective HBIG prophylaxis. [source] How to diagnose and treat hepatitis B virus antiviral drug resistance in the liver transplant settingLIVER TRANSPLANTATION, Issue S2 2008Anna S. F. Lok Key Points 1Hepatitis B virus variants with antiviral drug,resistant mutations and/or hepatitis B immune globulin,resistant mutations are the main cause of hepatitis B virus reinfections post,liver transplant. 2Early diagnosis of antiviral drug resistance and prompt initiation of rescue therapy are important in preventing hepatitis flares and hepatic decompensation. 3Virologic breakthrough is the first indication of antiviral drug resistance. 4Genotypic resistance testing should be performed when possible to avoid unnecessary modification of treatment in patients who do not have confirmed antiviral drug resistance and to permit appropriate selection of rescue therapy in those who have confirmed antiviral drug resistance. 5Choice of rescue therapy requires knowledge of the past history of hepatitis B virus treatments and virologic response to those treatments, patterns of mutations detected at the time of virologic breakthrough, and in vitro cross-resistance data. 6Occurrence of antiviral drug resistance can be reduced by the use of the most potent nucleos(t)ide analogue(s) with the highest genetic barrier to resistance, emphasis of medication compliance, and close monitoring of virologic response. Liver Transpl 14:S8,S14, 2008. © 2008 AASLD. [source] Prevention of recurrent hepatitis B post,liver transplantationLIVER TRANSPLANTATION, Issue 10B 2002Anna S.F. Lok MD 1Factors associated with a lower rate of recurrent hepatitis B post,liver transplantation (LT) are negative hepatitis B e antigen and/or serum hepatitis B virus DNA pre-LT, hepatitis D virus superinfection, and fulminant hepatitis B. 2Long-term intravenous hepatitis B immune globulin (HBIG) monotherapy can reduce the overall rate of recurrent hepatitis B to 20% to 35%. 3Long-term lamivudine monotherapy is associated with a risk for drug resistance and overall 3-year rate of recurrent hepatitis B of 40% to 50%. 4Combination prophylaxis with HBIG and lamivudine can reduce the overall rate of recurrent hepatitis B to 0% to 10%. 5The dose and duration of HBIG therapy needed when used in combination with lamivudine may be lower, but the optimal regimen remains to be determined. 6Lamivudine resistance before LT is associated with an increased risk for recurrent hepatitis B post-LT. 7A cost-effective prophylactic regimen to prevent recurrent hepatitis B should be tailored according to risk. [source] Late hepatic allograft dysfunctionLIVER TRANSPLANTATION, Issue 11B 2001Professor of Medicine Russell H. Wiesner MD Key Points 1Lifelong monitoring of graft function, immunosuppressive levels, and screening for drug toxicity is required in all liver recipients. 2Late hepatic allograft dysfunction is common and is caused by a variety of etiologies including rejection, infection, biliary/vascular abnormalities, recurrence of disease, and drug hepatotoxicity. 3In all patients with late hepatic allograft dysfunction, liver biopsy should be performed to assess for the presence of rejection, and to thus avoid excessive use of bolus corticosteroid therapy and guide appropriate immunosuppressive management. 4Recurrence of disease is the most common cause of late hepatic allograft dysfunction. 5Hepatitis C universally reinfects the hepatic allograft, and is associated with decreased patient and graft survival and leads to the recurrence of cirrhosis in 28% of patients within 5 years of transplantation. 6Major advances have been made in preventing recurrence of hepatitis B by the use of hepatitis B immune globulin in combination with lamivudine therapy. 7Autoimmune liver diseases such as primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis have a recurrence rate of approximately 20% to 30%. 8In patients developing recurrence of autoimmune hepatitis, steroid withdrawal is the most common cause. 9Recurrent hepatocellular cancer can be markedly reduced if strict guidelines are adhered to in selecting patients. 10Drug hepatotoxicity must always be considered in the differential diagnosis of late hepatic allograft dysfunction. [source] Lamivudine after hepatitis B immune globulin is effective in preventing hepatitis B recurrence after liver transplantationLIVER TRANSPLANTATION, Issue 4 2000S. Forrest Dodson MD The prevention of recurrent hepatitis B virus (HBV) infection after orthotopic liver transplantation (OLT) with hepatitis B immunoglobulin (HBIG) is expensive and requires indefinite parenteral administration. Lamivudine is a nucleoside analogue capable of inhibiting HBV replication. The aim of this study is to determine the efficacy of lamivudine in the prevention of recurrent HBV infection after a course of HBIG in patients who were hepatitis B surface antigen (HBsAg) positive and hepatitis Be antigen (HBeAg) negative before OLT. Patients at high risk for recurrent HBV infection (HBeAg positive and HBV DNA positive) were excluded. Thirty HBsAg-positive, HBeAg-negative patients underwent OLT from January 1993 to June 1997. All 30 patients were administered HBIG after OLT and, after 2 years, were given the option of continuing with HBIG or switching to lamivudine. Five patients were excluded: 3 patients were lost to follow-up and 2 patients died of technical complications. Three patients terminated HBIG therapy at 8, 24, and 29 months after OLT, and reinfection with HBV occurred in 1 patient. Six patients elected to continue HBIG therapy for life; 1 patient died of melanoma and the remaining 5 patients are HBsAg negative, with an average follow-up of 73 months. Sixteen patients were converted to lamivudine after a course of HBIG, and all 16 patients are HBsAg negative, with an average follow-up of 51 months after OLT. Five patients have been on lamivudine monotherapy for more than 24 months. These results suggest that lamivudine administered after a posttransplantation course of HBIG can effectively prevent the recurrence of HBV infection in patients who are HBsAg positive and HBeAg negative before OLT. [source] Deciphering antibody properties that lead to potent botulinum neurotoxin neutralizationMOVEMENT DISORDERS, Issue S8 2004James D. Marks MD Abstract Monoclonal antibodies (mAbs) have been developed that bind to the toxin binding domain (HC) of botulinum toxin type A. These mAbs recognize with high affinity nonoverlapping epitopes on native toxin. The potency of a combination of three of the mAbs is almost 100 times greater than that reported for human polyclonal botulinum immune globulin. Potency appears to result largely from a marked increase in binding affinity for toxin that results when antibodies are combined. Precise epitope, or even domain recognized, seems to be of much less importance. The very high affinity required for toxin neutralization suggests why single mAbs that potently neutralize toxin have not been reported. Such affinities are not typically generated by the immune response. © 2004 Movement Disorder Society [source] Kawasaki Disease with Facial Nerve ParalysisPEDIATRIC DERMATOLOGY, Issue 6 2003Margarita Larralde M.D., Ph.D. We describe an instance of facial nerve paralysis in a patient with KD. A 5-month-old boy developed fever, irritability, and diarrhea, treated 8 days later with cefaclor and ibuprofen. Three days later a confluent, erythematous and papular rash appeared, his lips were reddened and swollen, and his white blood count and platelet count were 20,900/mm3 and 558,000/mm3, respectively. He was admitted to the hospital with a diagnosis of KD, and an echocardiogram showed a right coronary aneurysm. The patient then developed an acute, right-sided, facial nerve peripheral paralysis that resolved over the next 6 weeks. He was treated with intravenous immune globulin (IVIG) 2 g/kg and aspirin 100 mg/kg/day with improvement of signs and symptoms. This report documents facial nerve paralysis as an uncommon complication of KD and points out that it may be a marker of increased risk of cardiovascular disease in this disorder. [source] Acute renal failure after intravenous anti-D immune globulin in an adult with immune thrombocytopenic purpuraAMERICAN JOURNAL OF HEMATOLOGY, Issue 4 2003Nancy S. Chun Abstract Intravenous anti-D immune globulin (anti-D IGIV) is indicated for the treatment of immune thrombocytopenic purpura (ITP) in nonsplenectomized patients who are Rh(D)-positive. Recent reports have described episodes of intravascular hemolysis (IVH) and acute renal failure (ARF) after anti-D IGIV. We report the first adult patient with ITP who required and received dialysis after IVH and ARF complicating treatment with anti-D IGIV. Whether the transfusion of 2 units of Rh(D)-positive red cells, indicated for the resulting anemia, exacerbated the IVH and renal failure is unclear. Three weeks after the administration of anti-D IGIV (13 days after two hemodialysis treatments), the patient's renal function had returned to normal. This case highlights the infrequent but potentially serious side effects of anti-D IGIV and the need to monitor a patient's renal function closely if there is evidence of IVH after infusion of anti-D IGIV. If red cell transfusion is indicated, we recommend the use of Rh(D)-negative red cell products. Am. J. Hematol. 74:276,279, 2003. © 2003 Wiley-Liss, Inc. [source] Impact of Virologic Breakthrough and HBIG Regimen on Hepatitis B Recurrence After Liver TransplantationAMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2010B. Degertekin The availability of hepatitis B immune globulin (HBIG) and several oral antiviral therapies has reduced but not eliminated hepatitis B virus (HBV) recurrence. We aimed to determine the rate of HBV recurrence after orthotopic liver transplantation (OLT) in relation to virologic breakthrough pre-OLT and HBIG regimens post-OLT. Data from the NIH HBV-OLT database were analyzed. A total of 183 patients transplanted between 2001 and 2007 followed for a median of 42 months (range 1,81) post-OLT were studied. At transplant, 29% were hepatitis B e antigen (HBeAg) (+), 38.5% had HBV DNA > 5 log10 copies/mL, 74% were receiving antiviral therapy. Twenty-five patients experienced virologic breakthrough before OLT. Post-OLT, 26%, 22%, 40% and 12% of patients received intravenous (IV) high-dose, IV low-dose, intramuscular low-dose and a finite duration of HBIG, respectively as maintenance prophylaxis. All but two patients also received antiviral therapy. Cumulative rates of HBV recurrence at 1 and 5 years were 3% and 9%, respectively. Multivariate analysis showed that listing HBeAg status and HBV DNA level at OLT were the only factors associated with HBV recurrence. In conclusion, low rates of HBV recurrence can be accomplished with all the HBIG regimens used when combined with antiviral therapy including patients with breakthrough pre-OLT as long as rescue therapy is administered pre- and post-OLT. [source] Virologic and Clinical Outcomes of Hepatitis B Virus Infection in HIV-HBV Coinfected Transplant RecipientsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 5 2010C. S. Coffin Liver transplantation (LT) is the treatment of choice for end-stage liver disease, but is controversial in patients with human immunodeficiency virus (HIV) infection. Using a prospective cohort of HIV-hepatitis B virus (HBV) coinfected patients transplanted between 2001,2007; outcomes including survival and HBV clinical recurrence were determined. Twenty-two coinfected patients underwent LT; 45% had detectable HBV DNA pre-LT and 72% were receiving anti-HBV drugs with efficacy against lamivudine-resistant HBV. Post-LT, all patients received hepatitis B immune globulin (HBIG) plus nucleos(t)ide analogues and remained HBsAg negative without clinical evidence of HBV recurrence, with a median follow-up 3.5 years. Low-level HBV viremia (median 108 IU/mL, range 9,789) was intermittently detected in 7/13 but not associated with HBsAg detection or ALT elevation. Compared with 20 HBV monoinfected patients on similar HBV prophylaxis and median follow-up of 4.0 years, patient and graft survival were similar: 100% versus 85% in HBV mono- versus coinfected patients (p = 0.08, log rank test). LT is effective for HIV-HBV coinfected patients with complications of cirrhosis, including those who are HBV DNA positive at the time of LT. Combination HBIG and antivirals is effective as prophylaxis with no clinical evidence of HBV recurrence but low-level HBV DNA is detectable in ,50% of recipients. [source] Characterization of Hepatitis B Virus Surface Antigen and Polymerase Mutations in Liver Transplant Recipients Pre- and Post-TransplantAMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2003Jeffrey J. Germer We evaluated serum samples from 18 chronic hepatitis B virus (HBV) patients who underwent liver transplantation for the presence of HBV polymerase and S gene mutations and HBV genotype using a new commercially available sequencing assay. All three patients with hepatitis B immune globulin (HBIG) treatment failure followed by nucleoside analogue treatment failure were infected with HBV genotype C; a pre-existing HBV S antigen (HBsAg) mutation (sD144A) was identified in one patient pretransplant, while sG145R mutations emerged in the other two patients post-transplant. These HBsAg mutations persisted for the duration of the study (5,6 years), despite the absence of HBIG administration for a 4,5-year period. Significant viral polymerase mutations (rtL180M and rtM204I/V) also emerged in all of these patients following treatment with lamivudine and/or famciclovir. Four of six patients with HBIG breakthrough without nucleoside analogue treatment failure yielded potentially significant HBsAg mutations post transplant. These data do not support previous reports highlighting the disappearance of HBsAg mutants in liver transplant recipients after discontinuation of HBIG. Determination of HBV genotype, as well as identification of HBV polymerase and S gene mutations in liver transplant candidates may be warranted to optimize HBV management strategies post transplant. [source] Successful treatment of human metapneumovirus pneumonia using combination therapy with intravenous ribavirin and immune globulinBRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2009Denise Bonney No abstract is available for this article. [source] Life-threatening human parvovirus b19 infection transmitted by intravenous immune globulin: reply to farrugiaBRITISH JOURNAL OF HAEMATOLOGY, Issue 6 2003Fumihiko Hayakawa No abstract is available for this article. [source] Subcutaneous administration of hepatitis B immune globulin in combination with lamivudine following orthotopic liver transplantation: effective prophylaxis against recurrenceCLINICAL TRANSPLANTATION, Issue 4 2006James J. Powell Abstract:, Prophylaxis against recurrent hepatitis B virus (HBV) infection with hepatitis B immune globulin (HBIG), in combination with antiviral agents such as lamivudine, has allowed transplantation for this condition to become feasible and accepted. Current protocols allow for HBIG administration either intravenously or intramuscularly. To date, there has been no reported experience with the subcutaneous route of post-transplant HBIG delivery. We report our experience of a 60-yr-old man for whom liver transplantation was performed for chronic HBV. HBIG was administered intramuscularly during the anhepatic phase of surgery. The finding of a portal vein thrombosis requiring repeated thrombectomy necessitated chronic anticoagulation. Post-operatively, HBIG was administered subcutaneously, in four separate injections, for a daily dose of 2170 IU along with continued lamivudine dosing. Hepatitis B surface antibody (anti-HBs) titres reached a serum concentration of >500 IU/L by seven d post-transplant and approximately 1000 IU/L by nine d post-transplant. Five months post-transplant, with continued combination of subcutaneous HBIG and lamivudine, there has been no recurrent HBV infection and anti-HBs titres have been at target levels. Our experience suggests that subcutaneous delivery of HBIG may be a feasible consideration when intramuscular/intravenous dosing is not possible. [source] Remnants of secondarily necrotic cells fuel inflammation in systemic lupus erythematosusARTHRITIS & RHEUMATISM, Issue 6 2009Luis E. Muñoz Objective Patients with systemic lupus erythematosus (SLE) are often characterized by cellular as well as humoral deficiencies in the recognition and phagocytosis of dead and dying cells. The aim of this study was to investigate whether the remnants of apoptotic cells are involved in the induction of inflammatory cytokines in blood-borne phagocytes. Methods We used ex vivo phagocytosis assays comprising cellular and humoral components and phagocytosis assays with isolated granulocytes and monocytes to study the phagocytosis of secondarily necrotic cell,derived material (SNEC). Cytokines were measured by multiplex bead array technology. Results We confirmed the impaired uptake of various particulate targets, including immunoglobulin-opsonized beads, by granulocytes and monocytes from patients with SLE compared with healthy control subjects. Surprisingly, blood-borne phagocytes from two-thirds of the patients with SLE took up SNEC, which was rarely phagocytosed by phagocytes from healthy control subjects or patients with rheumatoid arthritis. Supplementation of healthy donor blood with IgG fractions derived from patients with SLE transferred the capability to take up SNEC to the phagocytes of healthy donors. Phagocytosis-promoting immune globulins also induced secretion of huge amounts of cytokines by blood-borne phagocytes following uptake of SNEC. Conclusion Opsonization of SNEC by autoantibodies from patients with SLE fosters its uptake by blood-borne monocytes and granulocytes. Autoantibody-mediated phagocytosis of SNEC is accompanied by secretion of inflammatory cytokines, fueling the inflammation that contributes to the perpetuation of autoimmunity in SLE. [source] | ||||||||||||||||||||||||||||