Category: IMUNOLOGI

TLR mengaktifkan faktor transkripsi NFkB, AP-1, dan IRF

Last update: Oct 30, 2018

Pensinyalan TLR mamalia pada berbagai jenis sel menginduksi respon intrasel yang beragam, yang akhirnya dihasilkan berbagai sitokin inflamasi, faktor kemotaktik, peptida antimikroba, dan sitokin antiviral (interferon tipe I, dengan anggotanya IFN-alpha dan IFN-beta). Continue reading “TLR mengaktifkan faktor transkripsi NFkB, AP-1, dan IRF”

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Leukemia, limfoma, dan myeloma

Leukemia, limfoma, dan myeloma

Last update: May 28, 2018

Mari kita lihat tumor pada sistem imun.

Definisi

Leukemia berkembang di sumsum tulang. Ada sejumlah jenis leukemia yang berbeda. Tipe yang utama yaitu:

  • leukemia limfoblastik akut (acute lymphoblastic leukemia, ALL)
  • leukemia myeloid akut (acute myeloid leukemia, AML)
  • leukemia limfositik kronis (chronic lymphocytic leukemia, CLL)
  • leukemia myeloid kronis (chronic myeloid leukemia, CML).

Selanjutnya, ada subtipe dari masing-masing jenis leukemia ini. Continue reading “Leukemia, limfoma, dan myeloma”

Chapter 16 Manipulation of the immune response

Contents

  • Treatment of unwanted immune response (1-12)
  • Using the immune response to attack tumors (13-19)
  • Fighting infectious diseases with vaccination (20-31)

Detailed contents

  1. Corticosteroids are powerful anti-inflammatory drugs that alter the transcription of many genes.
  2. Cytotoxic drugs cause immunosuppression by killing dividing cells and have serious side-effects.
  3. Cyclosporin A, tacrolimus, rapamycin, and JAK inhibitors are effective immunosuppressive agents that interfere with various T-cell signaling pathway
  4. Antibodies against cell-surface molecules can be used to eliminate lymphocyte subsets or to inhibit lymphocyte function.
  5. Antibodies can be engineered to reduce their immunogenicity in humans.
  6. Monoclonal antibodies can be used to prevent allograft rejection.
  7. Depletion of autoreactive lymphocytes can treat autoimmune disease.
  8. Biologic agents that block TNF-a, IL-1, or IL-6 can alleviate autoimmune diseases.
  9. Biologic agents can block cell migration to sites of inflammation and reduce immune responses.
  10. Blockade of co-stimulatory pathways that activate lymphocytes can be used to treat autoimmune disease.
  11. Some commonly used drugs have immunomodulatory properties.
  12. Controlled administration of antigen can be used to manipulate the nature of an antigen-specific response.
  13. The development of transplantable tumors in mice led to the discovery of protective immune responses to tumors.
  14. Tumors are ‘edited’ by the immune system as they evolve and can escape rejection in many ways
  15. Tumor rejection antigens can be recognized T cells and form the basis of immunotherapies
  16. T cells expressing chimeric antigen receptors are an effective treatment in some leukemias
  17. Monoclonal antibodies against tumor antigens, alone or linked to toxins, can control tumor growth
  18. Enhancing the immune response to tumor by vaccination holds promise for cancer prevention and therapy
  19. Checkpoint blockade can augment immune responses to existing tumors
  20. Vaccines can be based on attenuated pathogens or material from killed organisms.
  21. Most effective vaccines generate antibodies that prevent the damage caused by toxins or that neutralize the pathogen and stop infection.
  22. Effective vaccines must induce long-lasting protection while being safe and inexpensive.
  23. Live-attenuated viral vaccines are usually more potent than ‘killed’ vaccines and can be made safer by the use of recombinant DNA technology.
  24. Live-attenuated vaccines can be developed by selecting nonpathogenic or disabled bacteria or by creating genetically attenuated parasites (GAPs).
  25. The route of vaccination is an important determinant of success.
  26. Bordetella pertussis vaccination illustrates the importance of the perceived safety of a vaccine
  27. Conjugate vaccines have been developed as a result of understanding how T and B cells collaborate in an immune response.
  28. Peptide-based vaccines can elicit protective immunity, but they require adjuvants and must be targeted to the appropriate cells and cell compartment to be effective.
  29. Adjuvants are important for enhancing the immunogenicity of vaccines, but few are approved for use in humans.
  30. Protective immunity can be induced by DNA-based vaccination.
  31. Vaccination and checkpoint blockade may be useful in controlling existing chronic infections.

 

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Chapter 15 Autoimmunity and transplantation

Contents

  • The making and breaking of self-tolerance (1-7)
  • Autoimmune diseases and pathogenic mechanisms (8-17)
  • The genetic and environmental basis of autoimmunity (18-28)
  • Responses to alloantigens and transplant rejection (29-38)

Detailed contents

  1. A critical function of the immune system is to discriminate self from nonself
  2. Multiple tolerance mechanisms normally prevent autoimmunity
  3. Central deletion or inactivation of newly formed lymphocytes is the first checkpoint of self-tolerance
  4. Lymphocytes that bind self antigens with relatively low affinity usually ignore them but in some circumstances become activated
  5. Antigens in immunologically privileged sites do not induce immune attack but can serve as targets
  6. Autoreactive T cells that express particular cytokines may be nonpathogenic or may suppress pathogenic lymphocytes
  7. Autoimmune responses can be controlled at various stages by regulatory T cells
  8. Specific adaptive immune responses to self antigens can cause autoimmune disease.
  9. Autoimmunity can be classified into either organ-specific or systemic disease.
  10. Multiple components of the immune system are typically recruited in autoimmune disease.
  11. Chronic autoimmune disease develops through positive feedback from inflammation, inability to clear the self antigen, and a broadening of the autoimmune response.
  12. Both antibody and effector T cells can cause tissue damage in autoimmune disease.
  13. Autoantibodies against blood cells promote their destruction.
  14. The fixation of sublytic doses of complement to cells in tissues stimulates a powerful inflammatory response.
  15. Autoantibodies against receptors cause disease by stimulating or blocking receptor function.
  16. Autoantibodies against extracellular antigens cause inflammatory injury
  17. T cells specific for self antigens can cause direct tissue injury and sustain autoantibody responses.
  18. Autoimmune diseases have a strong genetic component.
  19. Genomic-based approaches are providing new insight immunogenetic basis of autoimmunity
  20. Many genes that predispose to autoimmunity fall into categories that affect one or more of the mechanisms of tolerance.
  21. Monogenic defects of immune tolerance
  22. MHC genes have an important role in controlling susceptibility to autoimmune disease.
  23. Genetic variants that impair innate immune responses can predispose to T cell-mediated chronic inflammatory disease.
  24. External events can initiate autoimmunity.
  25. Infection can lead to autoimmune disease by providing ban environment that promotes lymphocyte activation.
  26. Cross-reactivity between foreign molecules on pathogens and self molecules can lead to anti-self responses and autoimmune disease.
  27. Drugs and toxins can cause autoimmune syndromes.
  28. Random events may be required for the initiation of autoimmune syndrome
  29. Graft rejection is an immunological response mediated primarily by T cells.
  30. Transplant rejection is caused primarily by the strong immune response to nonself MHC molecules.
  31. In MHC-identical grafts, rejection is caused by peptides from other alloantigens bound to graft MHC molecules.
  32. There are two ways of presenting alloantigens on the transplanted donor organ to the recipient’s T lymphocytes.
  33. Antibodies that react with endothelium cause hyperacute graft rejection.
  34. Late failure of transplanted organs is caused by chronic injury to the graft.
  35. A variety of organs are transplanted routinely in clinical medicine.
  36. The converse of graft rejection is graft-versus-host disease.
  37. Regulatory T cells are involved in alloreactive immune responses.

 

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Chapter 14 Allergy and allergic diseases

Contents

  • IgE and IgE-mediated allergic disease (1-5)
  • Effector mechanisms in IgE-mediated allergic disease (6-13)
  • Non-IgE-mediated allergic disease (14-17)

Detailed contents

  1. Sensitization involves class switching to lgE production on first contact with an allergen.
  2. Although many types of antigens can cause allergic sensitization, proteases are common sensitizing agents
  3. Genetic factors contribute to the development of lgE-mediated allergic disease.
  4. Environmental factors may interact with genetic susceptibility to cause allergic disease.
  5. Regulatory T cells can control allergic responses
  6. Most lgE is cell-bound and engages effector mechanisms of the immune system by pathways different from those of other antibody isotypes
  7. Mast cells reside in tissues and orchestrate allergic reactions.
  8. Eosinophils and basophils cause inflammation and tissue damage in allergic reactions.
  9. lgE-mediated allergic reactions have a rapid onset but can also lead to chronic responses.
  10. Allergen introduced into the bloodstream can cause anaphylaxis.
  11. Allergen inhalation is associated with the development of rhinitis and asthma.
  12. Allergy to particular foods causes systemic reactions as well as symptoms limited to the gut.
  13. lgE-mediated allergic disease can be treated by inhibiting the effector pathways that lead to symptoms or by desensitization techniques that aim at restoring tolerance to the allergen.
  14. Non-IgE dependent drug-induced hypersensitivity reactions in susceptible individuals occur by binding to the surfaces of circulating blood cells.
  15. Systemic disease caused by immune-complex formation can follow the administration of large quantities of poorly catabolized antigens.
  16. Hypersensitivity reactions can be mediated by TH1 cells and CD8 cytotoxic T cells.
  17. Celiac disease has features of both an allergic response and autoimmunity.

Chapter 13 Failures of host defense mechanisms

Contents

  • Immunodeficiency disease (1-18)
  • Evasion and subversion of immune defenses (19-24)
  • Acquired immune deficiency syndrome (25-38)

Detailed contents

  1. A history of repeated infections suggests a diagnosis of immunodeficiency.
  2. Primary immunodeficiency diseases are caused by inherited gene defects.
  3. Defects in cell development can result in severe combined immunodeficiencies.
  4. SCID can also be due to defects in the purine salvage pathway.
  5. Defects in antigen receptor gene rearrangement can result in SCID.
  6. Defects in signaling fromT-cell antigen receptors can cause severe immunodeficiency.
  7. Genetic defects in thymic function that block T-cell development result in severe immunodeficiencies.
  8. Defects in B-cell development result in deficiencies in antibody production that cause an inability to clear extracellular bacteria and some viruses
  9. Immune deficiencies can be caused by defects in B-cell or T-cell activation and function that lead to abnormal antibody responses
  10. Normal pathways for host defense against different infectious agent are pinpointed by genetic deficiencies of cytokine pathway centra to type 1/Th1 and type 3/Th17 responses
  11. Inherited defects in the cytolitic pathway of lymphocytes can cause uncontrolled lymphoproliferation and inflammatory responses to viral infections
  12. X-linked lymphoproliferative syndrome is associated with fatal infection by Epstein-Barr virus and with the development of lymphomas.
  13. Immunodeficiency is caused by inherited defects in the development of dendritic cell
  14. Defects in complement components and complement-regulatory proteins cause defective humoral immune function and tissue damage.
  15. Defects in phagocytic cells permit widespread bacterial infections.
  16. Mutation in the molecular regulators of inflammation can cause uncontrolled inflammatory responses that result in “autoinflammatory disease”
  17. Hematopoietic stem cell transplantation or gene therapy can be useful to correct genetic defects.
  18. Noninherited, secondary immunodeficiencies are major predisposing causes of infection and death
  19. Extracellular bacterial pathogens have evolved different strategies to avoid detection by pattern recognition receptors and destruction by antibody, complement, and antimicrobial peptides
  20. Intracellular bacterial pathogens can evade the immune system by seeking shelter within phagocytes
  21. Immune evasion is also practiced by protozoan parasites
  22. RNA viruses use different mechanisms of antigenic variation to keep ahead of the adaptive immune system
  23. DNA viruses use multiple mechanisms to subvert NK-cell and CTL responses
  24. Some latent viruses persist in vivo by ceasing to replicate until immunity wanes
  25. HIV is a retrovirus that establishes a chronic infection that slowly progresses to AIDS
  26. HIV infects and replicates within cells of the immune system
  27. Activated CD4 T cells are the major source of HIV replication
  28. There are several routes by which HIV is transmitted and establishes infection
  29. HIV variants with tropism for different co-receptors play different roles in transmission and progression of disease
  30. A genetic deficiency of the co-receptor CCR5 confers resistance to HIV infection
  31. An immune response controls but does not eliminate HIV
  32. Lymphoid tissue is the major reservoir of HIV infection.
  33. Genetic variation in the host can alter the rate of disease progression
  34. The destruction of immune function as a result of HIV infection leads to increased susceptibility to opportunistic infection and eventually to death.
  35. Drugs that block HIV replication lead to a rapid decrease in titer of infectious virus and an increase in CD4 T cells.
  36. In the course of infection HIV accumulates many mutations, which can result in the outgrowth of drug-resistant variants.
  37. Vaccination against HIV is an attractive solution but poses many difficulties.
  38. Prevention and education are important in controlling the spread of HIV and AIDS

 

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