Interferon alpha1 belongs to the type I interferon family and is encoded by the IFNA1 gene in humans. It is expressed in peripheral blood leukocytes and lymphoblastoid cells. It plays an important role in inducing non-specific resistance against a broad range of viral infections, and also affects cell proliferation and modulates immune responses. Interferon alpha proteins represent a group of related but distinct proteins that share over 95 % amino acid sequence homology. IFNA1 contains four highly conserved cysteine residues which form two disulfide bonds, one of which is necessary for biological activity. IFNalpha1A differs from IFNalpha1B by having one alanine residue in a position where IFNalpha1B has a valine.

Interferon alpha1 belongs to the type I interferon family and is encoded by the IFNA1 gene in humans. It is expressed in peripheral blood leukocytes and lymphoblastoid cells. It plays an important role in inducing non-specific resistance against a broad range of viral infections. It also affects cell proliferation and modulates immune responses. Interferon alpha proteins represent a group of related but distinct proteins that share over 95 % amino acid sequence homology. IFNA1 contains four highly conserved cysteine residues which form two disulfide bonds, one of which is necessary for biological activity. IFNalpha1B differs from IFNalpha1A by having one valine residue in a position where IFNalpha1A has an alanine.

Interferon alpha2 belongs to the type I interferon family and is encoded by the IFNA2 gene in humans. Like the other IFN-alpha proteins, it is expressed in leukocytes and plays an important role in inducing non-specific resistance against a broad range of viral infections. Recombinant IFN-alpha2A has been used to induce regression of corticosteroid-resistant hemangiomas in infancy. IFNA2 is one of 13 subtypes of interferon alpha found in humans, clustered on chromosome 9. It contains four highly conserved cysteine residues forming two disulfide bonds, one of which is necessary for biological activity.

Interferon alpha2 belongs to the type I interferon family and is encoded by the IFNA2 gene in humans. Like the other IFN-alpha proteins, it is expressed in leukocytes and plays an important role in inducing non-specific resistance against a broad range of viral infections. Studies have shown the ability of recombinant IFN-alpha2B to decrease hepatic metastases from intraocular melanoma. It used to treat high-risk cutaneous melanomas, but is associated with many contraindications. IFNA2 is one of 13 subtypes of interferon alpha found in humans, clustered on chromosome 9. It contains four highly conserved cysteine residues forming two disulfide bonds, one of which is necessary for biological activity.

Interferon alpha2 belongs to the type I interferon family and is encoded by the IFNA2 gene in humans. Like the other IFN-alpha proteins, it is expressed in leukocytes and plays an important role in inducing non-specific resistance against a broad range of viral infections. Studies have shown the ability of recombinant IFN-alpha2B to decrease hepatic metastases from intraocular melanoma. It used to treat high-risk cutaneous melanomas, but is associated with many contraindications. IFNA2 is one of 13 subtypes of interferon alpha found in humans, clustered on chromosome 9. It contains four highly conserved cysteine residues forming two disulfide bonds, one of which is necessary for biological activity.

Interferon gamma is the only type II interferon and binds to the heterodimeric IFNGR that consists of two chains, IFNGR1 and IFNGR2. This interaction activates the JAK-STAT pathway. IFNG is produced primarily by T-lymphocytes and natural killer (NK) cells. It is critical for innate and adaptive immunity against viral and intracellular bacterial infections. This is due partly to its ability to inhibit viral replication directly, but also due to its immunostimulatory and immunomodulatory effects. IFNG induces the production of cytokines and upregulates the expression of class I and II MHC antigens, Fc receptors, and leukocyte adhesion molecules. It modulates macrophage effector functions, influences isotype switching, and potentiates the secretion of immunoglobulins by B cells. Additionally, IFNG augments TH1 cell expansion and may be required for TH1 cell differentiation.

Interferon gamma is the only type II interferon and binds to the heterodimeric IFNGR that consists of two chains, IFNGR1 and IFNGR2. This interaction activates the JAK-STAT pathway. IFNG is produced primarily by T-lymphocytes and natural killer (NK) cells. It is critical for innate and adaptive immunity against viral and intracellular bacterial infections. This is due partly to its ability to inhibit viral replication directly, but also due to its immunostimulatory and immunomodulatory effects. IFNG induces the production of cytokines and upregulates the expression of class I and II MHC antigens, Fc receptors, and leukocyte adhesion molecules. It modulates macrophage effector functions, influences isotype switching, and potentiates the secretion of immunoglobulins by B cells. Additionally, IFNG augments TH1 cell expansion and may be required for TH1 cell differentiation.

Interferon gamma is the only type II interferon found in humans and binds to the heterodimeric IFNGR that consists of two chains, IFNGR1 and IFNGR2. This interaction activates the JAK-STAT pathway. IFNG is produced primarily by T-lymphocytes and natural killer (NK) cells. It is critical for innate and adaptive immunity against viral and intracellular bacterial infections. This is partly due to its ability to inhibit viral replication directly, but also due to its immunostimulatory and immunomodulatory effects. IFNG induces the production of cytokines and upregulates the expression of class I and II MHC antigens, Fc receptors, and leukocyte adhesion molecules. It modulates macrophage effector functions, influences isotype switching, and potentiates the secretion of immunoglobulins by B cells. Additionally, IFNG augments TH1 cell expansion and may be required for TH1 cell differentiation.

Interferon gamma is the only type II interferon and binds to the heterodimeric IFNGR that consists of two chains, IFNGR1 and IFNGR2. This interaction activates the JAK-STAT pathway. IFNG is produced primarily by T-lymphocytes and natural killer (NK) cells. It is critical for innate and adaptive immunity against viral and intracellular bacterial infections. This is due partly to its ability to inhibit viral replication directly, but also due to its immunostimulatory and immunomodulatory effects. IFNG induces the production of cytokines and upregulates the expression of class I and II MHC antigens, Fc receptors, and leukocyte adhesion molecules. It modulates macrophage effector functions, influences isotype switching, and potentiates the secretion of immunoglobulins by B cells. Additionally, IFNG augments TH1 cell expansion and may be required for TH1 cell differentiation.

Interferon gamma is the only type II interferon and binds to the heterodimeric IFNGR that consists of two chains, IFNGR1 and IFNGR2. This interaction activates the JAK-STAT pathway. IFNG is produced primarily by T-lymphocytes and natural killer (NK) cells. It is critical for innate and adaptive immunity against viral and intracellular bacterial infections. This is due partly to its ability to inhibit viral replication directly, but also due to its immunostimulatory and immunomodulatory effects. IFNG induces the production of cytokines and upregulates the expression of class I and II MHC antigens, Fc receptors, and leukocyte adhesion molecules. It modulates macrophage effector functions, influences isotype switching, and potentiates the secretion of immunoglobulins by B cells. Additionally, IFNG augments TH1 cell expansion and may be required for TH1 cell differentiation.

Interferon omega 1 is a member of the type I family of interferons. It is the only functional interferon omega gene in humans; many pseudogenes of interferon omega exist in humans, some of which are functional in non-primate placental mammals. Expression of IFNW1 is seen in leukocytes in response to viral infection or treatment with double-stranded RNA. It stimulates NK cell activity, enhances expression of major histocompatibility complex class I antigens, and inhibits proliferation of lymphocytes stimulated with mitogens or allogeneic cells. It also inhibits proliferation of a variety of tumor cell lines in vitro.