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Raja Md
-Raja Mohamed
-Amaraneni keerthi chowdary
-Neha zahed ali baig
-Amarawadi shiva kumar
-Sarfaraz ahmed
AUTOIMMUNE DISEASES
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
ETIOLOGY
• Unknown; It is thought to involve genetics together with environmental factors
PATHOGENESIS
CLINICAL MANIFESTATION
• Common initial and chronic complaints include fever, malaise, joint
pains, muscle pains, and fatigue.
• Neuropsychiatric syndromes can result when SLE affects central or
peripheral nervous system
TREATMENT
• Corticosteroids & immunosuppressive drugs
• cytotoxic drugs; Cyclophosphamide and Mycophenolate.
UV Radiation/ Environmental factor Apoptosis of cell Inadequate clearance in Nuclei Nuclear Antigen
Stimulate Lymphocytes
Production of Antibodies
Antibody-Antigen complex
Bind to Fc receptors in
B cells & Dendric cells
Autoantibodies Interferons & Cytokines
SJOGREN SYNDROME
ETIOLOGY
Genetic predisposition can be attributed to the alleles within the
major histocompatibility complex (MHC) class II gene region, in
particular HLA-DR and HLA-DQ alleles.
Environmental factors
infectious agents, particularly viruses.
PATHOGENESIS
CLINICAL MANIFESTATION
• Joint pain, swelling and stiffness & Swollen salivary gland
• Skin rashes or dry skin. Vaginal dryness.
• Extraarticular manifestations including mixed cryoglobulinemia.
TREATMENT
Hydroxychloroquine
Surgery A minor procedure to seal the tear ducts that drain tears from our eyes might help relieve our dry eyes
Viral Infection trigger on Salivary gland Cell death & Tissue self Antigen
Genetically Susceptible Individual CD4+ T Cells CD4+ B Cells
Escape
tolerance
Inflammation, Tissue damage & Fibrosis
&
SYSTEMIC SCLEROSIS
ETIOLOGY
Unknown
PATHOGENESIS
CLINICAL MANIFESTATION
• Atypical chest pain, fatigue, dyspnoea, hypertension, Joint pain, limitation of movement, joint swelling, and muscle pain
TREATMENT
• Calcium-channel blockers, vasodilating drugs, intravenous prostaglandins, prostacyclin analogs or aspirin
CD4+ T Cells Cytokines
TGF-β & IL-13
Stimulate transcription of genes that encode collagen
& other extracellular matrix protein in Fibroblast
Mixed Connective Tissue Disease
ETIOLOGY
The causes of MCTD are not known. It is not directly inherited
PATHOGENESIS
 characterized by the presence of elevated blood levels of a specific
autoantibody, now called anti-U1 ribonucleoprotein (RNP)
 RNP is immunologically protected due to its location, however if a cell dies
and RNP is no longer contained in the nucleus and thus unprotected, the
immune system can respond by forming antibodies due to cellular mimicry.
TREATMENT
Corticosteroids.
Ii’s defined as a connective tissue disorder characterized by the
presence of high titer antibodies to ribonucleoprotein
combination with clinical features commonly seen in systemic
lupus erythematosus scleroderma and polymyositis
IgG4 Related Disease
Infiltrate dominated by IgG4 antibodies-producing cells, lymphocytes
,increase serum IgG4
CLINICAL MANIFESTATION
• IgG4-related disease (IgG4-RD) can involve one or multiple
organs.
• diffuse enlargement of an organ (eg, the pancreas) , periorbital
tissue, breasts, kidneys
• Mikulicz syndrome , riedel thyroiditis
TREATMENT
 Glucocorticoids are cornerstone therapy for this
condition
 use low dose 5–7.5 mg of prednisone equivalent
for maintenance therapy.
 Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is a chronic, systemic,
inflammatory condition
TRANSPLANT REJECTION
Transplant rejection occurs when transplanted tissue is rejected by the recipient's
immune system, which destroys the transplanted tissue
CLINICAL MANIFESTATIONS
Pain at the site of the transplant ,Feeling unwell Fatigue/lack of
energy, Flu-like symptoms, Fever ,Weight changes, Swelling,
Change in heart rate, Urinating less often
TREATMENT
corticosteroids can be applied
Hyperacute rejection manifests severely and within minutes, and so treatment is immediate: removal of the tissue.
Chronic rejection is generally considered irreversible and poorly amenable to treatment—only retransplant
generally indicated if feasible—though inhaled ciclosporin is being investigated to delay or prevent chronic
rejection of lung transplants. Blood transfer Marrow transplant Antibody based treatments Gene therapy
REJECTION REACTIONS ARE CLASSIFIED AS:-
1. Hyperacute rejection
2. Acute rejection
3. Chronic rejection
THANK YOU

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Understanding Autoimmune Diseases

  • 1. Raja Md -Raja Mohamed -Amaraneni keerthi chowdary -Neha zahed ali baig -Amarawadi shiva kumar -Sarfaraz ahmed AUTOIMMUNE DISEASES
  • 2. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) ETIOLOGY • Unknown; It is thought to involve genetics together with environmental factors PATHOGENESIS CLINICAL MANIFESTATION • Common initial and chronic complaints include fever, malaise, joint pains, muscle pains, and fatigue. • Neuropsychiatric syndromes can result when SLE affects central or peripheral nervous system TREATMENT • Corticosteroids & immunosuppressive drugs • cytotoxic drugs; Cyclophosphamide and Mycophenolate. UV Radiation/ Environmental factor Apoptosis of cell Inadequate clearance in Nuclei Nuclear Antigen Stimulate Lymphocytes Production of Antibodies Antibody-Antigen complex Bind to Fc receptors in B cells & Dendric cells Autoantibodies Interferons & Cytokines
  • 3. SJOGREN SYNDROME ETIOLOGY Genetic predisposition can be attributed to the alleles within the major histocompatibility complex (MHC) class II gene region, in particular HLA-DR and HLA-DQ alleles. Environmental factors infectious agents, particularly viruses. PATHOGENESIS CLINICAL MANIFESTATION • Joint pain, swelling and stiffness & Swollen salivary gland • Skin rashes or dry skin. Vaginal dryness. • Extraarticular manifestations including mixed cryoglobulinemia. TREATMENT Hydroxychloroquine Surgery A minor procedure to seal the tear ducts that drain tears from our eyes might help relieve our dry eyes Viral Infection trigger on Salivary gland Cell death & Tissue self Antigen Genetically Susceptible Individual CD4+ T Cells CD4+ B Cells Escape tolerance Inflammation, Tissue damage & Fibrosis &
  • 4. SYSTEMIC SCLEROSIS ETIOLOGY Unknown PATHOGENESIS CLINICAL MANIFESTATION • Atypical chest pain, fatigue, dyspnoea, hypertension, Joint pain, limitation of movement, joint swelling, and muscle pain TREATMENT • Calcium-channel blockers, vasodilating drugs, intravenous prostaglandins, prostacyclin analogs or aspirin CD4+ T Cells Cytokines TGF-β & IL-13 Stimulate transcription of genes that encode collagen & other extracellular matrix protein in Fibroblast
  • 5. Mixed Connective Tissue Disease ETIOLOGY The causes of MCTD are not known. It is not directly inherited PATHOGENESIS  characterized by the presence of elevated blood levels of a specific autoantibody, now called anti-U1 ribonucleoprotein (RNP)  RNP is immunologically protected due to its location, however if a cell dies and RNP is no longer contained in the nucleus and thus unprotected, the immune system can respond by forming antibodies due to cellular mimicry. TREATMENT Corticosteroids. Ii’s defined as a connective tissue disorder characterized by the presence of high titer antibodies to ribonucleoprotein combination with clinical features commonly seen in systemic lupus erythematosus scleroderma and polymyositis
  • 6. IgG4 Related Disease Infiltrate dominated by IgG4 antibodies-producing cells, lymphocytes ,increase serum IgG4 CLINICAL MANIFESTATION • IgG4-related disease (IgG4-RD) can involve one or multiple organs. • diffuse enlargement of an organ (eg, the pancreas) , periorbital tissue, breasts, kidneys • Mikulicz syndrome , riedel thyroiditis TREATMENT  Glucocorticoids are cornerstone therapy for this condition  use low dose 5–7.5 mg of prednisone equivalent for maintenance therapy.  Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is a chronic, systemic, inflammatory condition
  • 7. TRANSPLANT REJECTION Transplant rejection occurs when transplanted tissue is rejected by the recipient's immune system, which destroys the transplanted tissue CLINICAL MANIFESTATIONS Pain at the site of the transplant ,Feeling unwell Fatigue/lack of energy, Flu-like symptoms, Fever ,Weight changes, Swelling, Change in heart rate, Urinating less often TREATMENT corticosteroids can be applied Hyperacute rejection manifests severely and within minutes, and so treatment is immediate: removal of the tissue. Chronic rejection is generally considered irreversible and poorly amenable to treatment—only retransplant generally indicated if feasible—though inhaled ciclosporin is being investigated to delay or prevent chronic rejection of lung transplants. Blood transfer Marrow transplant Antibody based treatments Gene therapy REJECTION REACTIONS ARE CLASSIFIED AS:- 1. Hyperacute rejection 2. Acute rejection 3. Chronic rejection