Module 1 Immunity Fall 2024 PDF

Copyright © 2021 by Jones and Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com TWO- CHAPTER IMMUNITY STRESS Physiological response to stress Universal experience, results from positive or nega...

Copyright © 2021 by Jones and Bartlett Learning, LLC an Ascend Learning Company. www.jblearning.com TWO- CHAPTER IMMUNITY STRESS Physiological response to stress Universal experience, results from positive or negative experiences A body response to change May negatively impact homeostasis  STRESS: THE STRESS RESPONSE General adaptation syndrome: ⚬Alarm stage ⚬Resistance stage ⚬Exhaustion stage Local adaptation syndrome: ⚬Confines damage to one area Stress response is somewhat predictable with individual variability ⚬Conditioning factors: genetics, age, gender, history, and support ⚬Some coping strategies can minimize effects ⚬Other strategies cause more problems than benefits EFFECTS OF STRESS IMMUNITY BODY CONSTANTLY UNDER ASSAULT BY MICROBES IMMUNE SYSTEM IS SELF- REGULATED AND SELF- LIMITING ⚬Must be able to distinguish self from nonself ⚬Antigens TWO KEY ACTIVITIES: DEFENSE AND ATTACK  Barriers ⚬Nonspecific but immediate: recognizes nonself but not specific pathogens ⚬Includes skin and mucous membranes, chemicals, and microbiome ⚬Not completely impenetrable Inflammatory response ⚬Vascular reaction from damage or trauma to body tissue (mast cells trigger) ⚬Nondiscriminatory: same sequence INNATE VERSUS regardless of cause, local and systemic ⚬Acute phase: immediately after injury, until ADAPTIVE threat is eliminated ⚬Vasodilation and vasoconstriction, IMMUNITY: phagocytosis, fibrinogen ⚬Chronic phase: if acute does not resolve issue, lasts until healing is complete ⚬Chronic often occurs in presence of INNATE resistant organisms  Pyrogens ⚬Released by bacteria or after exposure INNATE ⚬Cause systemic inflammatory response (fever) which can be life-threatening VERSUS ⚬Make unfavorable environment for bacterial proliferation ADAPTIVE Interferons IMMUNIT ⚬Released from virus-infected cells, they bind to uninfected cells Y: ⚬Uninfected cells release an enzyme that prevents viral replication Complement proteins INNATE ⚬Plasma proteins enhance antibodies ⚬Activated by antigens IMMUNIT ⚬Play a role in immune/inflammatory response INNATE VERSUS ADAPTIVE IMMUNITY: ADAPTIVE DEFENSES Also known as acquired defenses, they pursue those who escape innate defenses Specific to organisms (have memory that develops over time) Distinguishes self/nonself and between each pathogen Cellular immunity (destroy the antigen) ⚬T cells: regulator cells (helper T and suppressor T) and effector cells (cytotoxic killer T cells) are produced in marrow and mature in thymus ⚬Four types of Th (helper) cells ⚬Viruses and cancer; hypersensitivity and transplant rejection Humoral immunity (produce antibodies against the antigen) ⚬B cells: memory cells and immunoglobulin-secreting cells produce antibodies 72 hours after initial exposure ⚬Memory cells: quicker response to same antigen in the future ⚬Active and passive acquired immunities  Immunity in infancy ⚬Breastfeeding can transfer IgA; is based on maternal vaccinations grant additional protection INNATE IgG for 3 to 6 months, granting ⚬Newborns can only respond effectively temporary passive to protein antigens, not glycoproteins or VERSUS immunity, but polysaccharides, and many immune transferred functions are limited antibodies have low ADAPTIV affinity In adolescence, ⚬Risk for inflammatory and E hormonal changes impact the immune autoimmune diseases increases IMMUNIT system as B cells ⚬Immune dimorphism (the sexes and macrophages have hormone respond differently to Y: receptors infection/vaccination) ⚬Lower B- and T-cell production, but increased apoptosis of these cells IMMUNIT Age decreases immune response ⚬Age-related changes are multifactorial in immune Y ACROSS ⚬Comorbidity significantly impacts immunity senescence and autoimmune disorders become more likely due to misinterpretation of signals flooding the body  Type I Type II Type III Type IV Type I (IgE Type II (cytotoxic Type III (immune Type IV (delayed hypersensitivity): mediated): immediate (usually); complex-mediated): hypersensitivity): immediate; local or targets single cell delayed; local or delayed, two systemic ⚬IgG or IgM antibodies systemic phases: sensitizing bind to antigen on ⚬Circulating antigen- individual’s own cells, and effector ⚬Occurs when T- antibody complexes triggering antibody helpers stimulate B production in accumulate in ⚬Cell-mediated (T cells to produce IgE macrophages tissue, triggering the cells), not antibody- that sensitizes mast ⚬Cell lysis occurs due to complement mediated; antigen cells and basophils; activation of system’s presentation results requires repeated complement and inflammatory phagocytosis in cytokine release, exposure to large response severe tissue injury, doses of allergen and fibrosis INNATE VERSUS ADAPTIVE IMMUNITY: ALTERED IMMUNE RESPONSE: HYPERSENSITIVITY HYPERSENSITIVI TY CONTINUED IgE- produced by immune system during response to allergen IgG and IgM- causes cellular destruction, functional loss, damage to tissues (immune system attacks the body’s own cells or tissues) Immune complex- antibody binds to antigen, can cause complement activation, anaphylaxis T-cells- white blood cells (cytotoxic t-cells and helper t-  TYPE II HYPERSENSITIVITY Blood Transfusion Erythroblastosis Reactions Fetalis  TYPE IV HYPERSENSITIVI TY Exposure to hapten antigens in poison ivy can cause contact dermatitis, a type IV hypersensitivity. (A) The first exposure to poison ivy does not result in a reaction. However, sensitization stimulates helper T cells, leading to the production of memory helper T cells that can become reactivated on future exposures. (B) On secondary exposure, the memory helper T cells become reactivated, producing inflammatory cytokines that stimulate macrophages and cytotoxic T cells to induce an inflammatory lesion at the exposed site. This lesion, which will A B persist until the allergen is removed, can inflict significant tissue damage if it remains present for a long enough period.  TRANSPLANT REACTIONS Success requires the best match of tissue antigens from a living or nonliving donor Four types of transplants: ⚬Allogeneic: donor/recipient are related or unrelated, similar tissue types; most common ⚬Syngeneic: donor/recipient are identical twins ⚬Autologous: donor/recipient are same person (most successful method) ⚬Xenogenic: donor/recipient are different species Responses to transplant: ⚬Hyperacute tissue rejection: nearly immediate, due to complement system, causes necrosis ⚬Acute tissue rejection: occurs within 3 months, is treatable, and manifests in fever, edema, etc. ⚬Chronic tissue rejection: from 4 months on, antibody-mediated, due to ischemia in vessel walls of transplanted tissue Host vs. graft disease or graft vs. host disease: either tissue may have immune response ⚬Either may be treated with lifelong immunosuppression if the tissue is a match  AUTOIMMUNITY Immune system cannot recognize itself and www.jblearning.com Copyright © 2021 by Jones and Bartlett Learning, LLC an Ascend Learning Company. mounts immune response against self Triggering mechanism is unclear, but affects any tissue Known predictors: genetics, female sex, abnormal stressors Frequently progressive relapsing-remitting disorders with periods of exacerbation and remission Diagnosis often attempts to eliminate all other possibilities AUTOIMMUNITY: SYSTEMIC LUPUS ERYTHEMATOSUS Chronic stress-related inflammatory condition affecting connective tissue Can be mild or severe, potentially due to B cells producing autoantibodies and autoantigens Stressors tend to trigger exacerbations More common in women, Asians, and African Most often harms the heart, joints, Americans skin, lungs, blood vessels, liver, kidneys, and nervous system  AUTOIMMUNITY: IMMUNODEFICIENCY Diminished or absent immune response increases vulnerability to opportunistic infections May be acute or chronic Primary (defect with the immune system) or Secondary (underlying disease or factor this is suppressing immune system)  Acquired Immunodeficiency Syndrome (AIDS) Human immunodeficiency virus (HIV) ⚬Retrovirus infecting CD4 and macrophages (requires a host to survive) ⚬Transmitted via blood and bodily fluids; expecting mothers risk infecting their child ⚬Not transmitted through saliva ⚬HIV-1 is the most prevalent strain in the United States Asymptomatic phase allows the virus to reproduce for several years ⚬As viral load rises, CD4 is destroyed and symptoms increase in severity Progression has three potential forms: ⚬Immunodeficiency (opportunistic infections) ⚬Autoimmunity (e.g., arthritis) ⚬Neurologic dysfunction (e.g., AIDS dementia complex)  Diagnostic tests help determine progression, with higher viral load indicating further clinical progression: ⚬Nucleic acid tests (NAT): detects viral load, but is expensive and nonroutine ⚬Antigen/antibody tests: often administered with NAT, come in rapid and home versions to detect antigen p24 in blood or saliva Lab-based categorization derived from CD4 cell count: (lower CD4, more severe) ⚬Category 1: > 500 cells/μL AIDS- ⚬Category 2: 200–499 ⚬Category 3: < 200 CONTINUE D Categorization based on clinical presentation: ⚬Category A: asymptomatic ⚬Category B: some less-serious manifestations of immunodeficiency ⚬Category C: AIDS-defining illnesses present  DEVELOPING A STRONG IMMUNE SYSTEM Avoid Smoking oversanitizing the cessation and environment to moderate alcohol Exercise Vaccinations build immunity consumption Getting Increased fluid Well-balanced Weight adequate intake diet management sleep Reducing stress