Immune Gamma

[Ottavia Delamar]

Somepeople may take IVIg instead of other medications (such as immunosuppressants, corticosteroids, or biologic drugs) to help treat their immune system disorders. In some cases, you may take IVIg along with immunosuppressants or other meds.

Liquid immunoglobulin is taken from the blood plasma of donors who are screened to make sure they are healthy. The plasma is tested for serious infections like hepatitis and AIDS. The plasma is purified before it's used for IVIg therapy.

During the therapy, prepared immunoglobulin is infused into your veins. A health care provider uses a needle to get into your vein. Then the medicine can flow from a bag through a tube into your arm. This takes about 2 to 4 hours.

Typically you'll have treatments every 3 to 4 weeks to keep your immune system strong. Your blood may break down about half of the immunoglobulin over that period, so you'll need another dose to keep fighting infections.

You might feel your best soon after your treatment, when the highest amount of immunoglobulin is in your body. As your body absorbs it , though, you may start to feel more weak or tired. You might feel your worst just before your next treatment.

If you have severe side effects from IVIg, you might be able to switch to another type of treatment called subcutaneous immunoglobulin therapy, or SCIG. You'd get shots with small amounts of immunoglobulin under your skin either once a week or every few days. Talk to your doctor about your treatment options.

At ACTIMMUNE.com, you can learn more about the signs and symptoms of chronic granulomatous disease (CGD). You can find information on how ACTIMMUNE helps protect against serious infections and hear from patients and caregivers about living with CGD and taking ACTIMMUNE.

You can also download helpful resources that explain CGD and get tips to help you start and stay on ACTIMMUNE for CGD. Another resource to help you at every step is a Clinical Nurse Educator, available at no cost. Sign up for more information and valuable tips about ACTIMMUNE to help treat CGD.

ACTIMMUNE is part of a drug regimen used to treat Chronic Granulomatous Disease, or CGD. CGD is a genetic disorder, usually diagnosed in childhood, that affects some cells of the immune system and the body's ability to fight infections effectively. CGD is often treated (though not cured) with antibiotics, antifungals, and ACTIMMUNE.

ACTIMMUNE is also used to slow the worsening of severe, malignant osteopetrosis (SMO). SMO is a genetic disorder that affects normal bone formation and is usually diagnosed in the first few months after birth.

ACTIMMUNE may cause decreased mental status, walking disturbances, and dizziness, particularly at very high doses. These symptoms are usually reversible within a few days upon dose reduction or discontinuation of therapy.

Bone marrow function may be suppressed with ACTIMMUNE, and decreased production of cells important to the body may occur. This effect, which can be severe, is usually reversible when the drug is discontinued or the dose is reduced.

Taking ACTIMMUNE may cause reversible changes to your liver function, particularly in patients less than 1 year old. Your doctor should monitor your liver function every 3 months, and monthly in children under 1 year.

The most common side effects with ACTIMMUNE are "flu-like" symptoms such as fever, headache, chills, muscle pain, or fatigue, which may decrease in severity as treatment continues. Bedtime administration of ACTIMMUNE may help reduce some of these symptoms. Acetaminophen may be helpful in preventing fever and headache.

Some drugs may interact with ACTIMMUNE to potentially increase the risk of damage to your heart or nervous system, such as certain chemotherapy drugs. Tell your doctor about all other medications you are taking.

The risk information provided here is not comprehensive. To learn more, talk about ACTIMMUNE with your healthcare provider or pharmacist. The FDA-approved product labeling can be found at or 1-866-479-6742.

The information provided in this site is intended only for residents of the United States. The health information contained herein is provided for educational purposes only and is not intended to replace discussions with a healthcare provider.

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Immune gamma globulin (IgG) has a long history in the treatment of both primary immune deficiency and autoimmune disorders. Disease indications continue to expand and new-generation products increase the versatility of delivery. This review encompasses a historical perspective as well as current and future implications of human immune globulin for the treatment of immune-mediated illness.

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Mtb infection is acquired primarily via aerosol transmission through close contact with an individual with pulmonary TB. Nevertheless, in household contact studies not all individuals with high levels of Mtb exposure become infected, as measured by TST and IGRA9. In the present study we aimed to more fully characterize the immune responses to Mtb in these individuals to determine whether they are truly non-reactive to Mtb or, alternatively, have non-canonical responses after exposure.

Mendelian defects in IFN-γ production or signaling are associated with increased susceptibility to mycobacterial infections32, and studies in mice demonstrate the importance of IFN-γ in controlling Mtb infection33,34,35,36,37,38. However, several examples reveal IFN-γ-independent control of Mtb infection or even an antagonistic role for IFN-γ39,40,41. Moreover, in BCG-vaccinated children, low-level IFN-γ-producing T cells do not represent an immunologic correlate of risk for the development of TB42 and IFN-γ T cell immunity failed to predict protection against progression to Mtb disease after MVA85A vaccination, known to induce strong IFN-γ responses43. Indeed, ESAT6-specific T cells have been shown to control Mtb infection in the absence of IFN-γ and TNF39. Thus immune factors beyond IFN-γ and classic Th1 immunity may provide protection against Mtb disease.

The raw ICS data were compensated for and manually gated using FlowJo (TreeStar Inc.). A representative gating tree is shown in Extended data Fig. 9. The data were then processed using the OpenCyto framework in the R programming environment62. Although we began with 25 subjects for each group, samples with poor viability defined on the basis of low CD3 counts (

L.L.L., C.S. and G.A. conceived and planned experiments. L.L.L., K.K.Q.Y., P.S.G., A.C. and T.M. performed the experiments and analyzed the data. M.T.S., W.H.Y. and D.L. facilitated computational analyses. C.M.S., H.M.-K., T.R.H. and W.H.B. contributed epidemiologic analysis and established the clinical cohorts. L.L.L., C.S., S.M.F. and G.A. wrote the manuscript, with contributions from M.T.S., K.K.Q.Y., C.L., T.J.S., P.S.G., A.C., W.H.Y., T.M., R.D.C., D.L., H.M.-K., T.R.H., W.H.B. and C.M.S.

a, Variability between technical replicates in customized Luminex are shown by a representative dataset of ESAT6/CFP10 specific IgG MFI readings. b, Variability between technical replicates in Fc-effector functional assays are shown by a representative dataset of ESAT6/CFP10 specific antibody-dependent cellular phagocytosis scores. c, Variability between two different donors in NK cell activation is shown by percentage Mip1b positive from Donor C and Donor D. Correlations are determined by Spearman rank with P values as indicated.

A representative gating tree for flow analysis of cells following stimulation with antigen. Gating (top row) began with singlets, followed by viable cells. Lymphocytes were then identified by size, and CD3 expression was used to focus on T cells. The T cells were then separated into CD4 versus CD8 co-receptor subsets. For each subset (CD4 middle row, CD8 bottom row), cytokines were visualized by gating against IFN-γ. Pink boxes demonstrated positive staining. Positivity of cytokines was determined by DMSO negative and SEB positive controls as well as by gating on CD3 negative populations (not shown). Gating for CD4 and CD8 cytokines was determined separately.

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