Chapter 5 Diseases of immunity

Nonspecific immunity- do not require previous contact with a specific

microorganism
● physical barriers
● Antibacterial Agents
● Commensal Microorganisms
● Ongoing Phagocytosis
● Inflammatory Response
● Fever

Specific Immunity- required after birth

· Recognition-discovering a new pathogen
· Learning- what to do when there is a second or subsequent exposure
to pathogen
· Memory- improved response to pathogen
· Self-discrimination- able to discriminate between foreign substances
and those that make up our own body, and to direct its attack only against
intruders
Lymphocytes
T-Lymphocytes
o Produced in bone marrow or thymus( mature here)
o T-cell receptors recognize antigens and immunogenic
o Able to recognize foreign substances particularly the surface features of
microorganisms, because their receptor shapes match, allowing them to bind
together.
o Antigenic Determinants or epitopes – the billions of binding sites for the
T-cell
§ Why we may have an allergic response to something harmless
§ May confuse nonself-antigens with self-antigens
o Are looking for trouble from foreign substances
· B-Lymphocytes
o Antibody producing cells
o Mature in the bone marrow
o React to specific epitopes
o Antibodies- y shaped linkers who limit repertoire of defenses to the host
of invaders that threaten us
§ Antigen-binding fragment (FAB)- can attach and mark any of a billion
epitopes; and can neutralize toxic substances
§ The Fc (crystallizable fragment)- the stalk of the Y, this will bring about the
production of masses of antigen-specific antibodies that can bind to the
antigen
· Macrophages, PMNs and eoxinophils have Fc receptors
o These antibodies produce a first line of defense:
§ IgM- a normal immune response
§ IgG- most prevalent in blood
§ IgE-allergies and worms
§ IgA- GI related (gut checker)
§ IgD- antigen receptor on lymphocyte membranes
· Natural killer cells (NK cells)
o Large granular lymphocytes that are killers of foreign substances
o Antibody-dependent cellular cytotoxicity (ADCC) shared with
neutrophils, macrophages, and eosinophils
o Tumor surveillance- recognize if a cell is becoming abnormal, then
engage and kill it
Lymphoid Tissue
· Primary- red bone marrow and thymus, where T & B lymphocytes are
formed
· Secondary- lymph nodes, spleen, tonsils, Peyer’s patches in the
intestines
o Draining lymph enters blood circulation then can reenter other
secondary lymphoid tissues
o The lymphoid tissue are strategically placed to locate and encounter
antigens shortly after it violates the body’s outer defenses
o Lymphocyte traffic increases chances of running into an antigen in the
body
§ Filter
Immune Response
· A macrophage is usually a quick responder to foreign substance
o Once it has destroyed a foreign substance , the antigens, are then
displayed on the surface of the macrophage, which presents them to T cells
o Of the T-cells, one will have T-cell receptor that corresponds to an
epitope of the antigen
o This T-cell is called a helper T cell (Th cell) matching this th cell is called
clonal selection
o The Th cell is activated into clonal expansion along with memory cells
§ Cytotoxic T cells are activated which can identify and kill virus- or parasite
infected cells
§ With the expansion of Th cells it initiates the movement of NK cells &
macrophages
o Antigen presenting cells stimulate B-cells (starting with IgM and then
IgG) to produce antibodies and form memory cells allowing for faster
response to the antigen in the future
o Cytotokines is a mediating factor that will communicate between cells
§ Stimulates nearby immune cells to become active and promote
inflammation
o Overview of Immune response
 § Figure 5.12

Immunization – is the preventive technique of artificially inducing an immune response. It

stimulates the immune system without exposing it to an infection. Inducing a toxins antigenic
component is known as a vaccine

· The purpose of a vaccine is to induce a primary antibody response with the long-term
retention provided by memory T and B cells.
· Measles, Mumps, Rubella are immunized with attenuated viruses (children 15-19 months
old)
· Diphtheria is immunized with diphtheria toxoid and Pertussis, Tetanus are immunized with
bordetella pertussis, tetanus toxoid (children 2-3 months old)
Vaccine induced immunities are said to be active and passive immunity is ready made
antibodies from outside the system.

Hypersensitivity - reactions involve deleterious effects caused by the immune system

resulting in tissue damage. There are four types of reactions.
· Type 1 – Immediate hypersensitivity : Contact with antigen results in plasma cell
production of IgE antibody. This binds to the Fc receptors on mucosal, dermal, or perivascular
mast cells, thus arming them. This results in mast cell degranulation and synthesis of secondary
mediators. Primary mediator of mast cell degranulation is histamineTypical manifestations
include hay fever, asthma, hives, food allergies, and eczema.
· Type 2 – Cytotoxic Hypersensitivity : Ab directed against cell surface antigens mediates
cell destruction via complement activation. Includes blood transfusion reactions, autoimmune
hemolytic anemia.
· Type 3 - Complex-Mediated Hypersensitivity : Induce complement activation and
ensues inflammatory response mediated by massive infiltration of neutrophils. Includes serum
sickness, rheumatoid arthritis, and systemic lupus erythematosus
· Type 4 – Cell-mediated Hypersensitivity : Cytokines that activate macrophages or Tc
cells which mediate direct cellular damage. Includes dermatitis, tubercular lesions, and graft
rejection
· Graft rejection : Antigen presenting cells facilitate T-cell sensitization, which enhances
complement deposition and platelet aggregation and in turn phagocytosis. Antibody binding
makes possible antibody-dependent cellular cytotoxicity by NK cells. NK cells attack the
transplant tissue, while sensitized and activated T cells mobilize a chronic attack on the graft
tissue.
Primary Immune Deficiencies – result when one or more components of immune system
function are deficient or lacking, often because of a genetic defect, with a resulting characteristic
pattern of infection.
· B-cell deficiencies result in recurrent infections by viruses that are normally neutralized by
antibody or bacteria that can resist phagocytosis. This B-cell deficit produces lower
gammaglobulin levels.
· T-cell deficiencies result in chronic or recurrent infections with viruses, yeast, intracellular
bacteria. DiGeorge syndrome is a disorder of various nonimmune abnormalities, such as, small
jaw and cheeks, turned-down mouth, heart defects.
Secondary Immune Deficiencies – can arise from a wide variety of infections or as a toxic
effect of drugs or other medical treatments.

HIV Events
· “Doesn’t play by the rules”
o Carries RNA not DNA also has reverse transcriptase
o Gp 120 proteins bind to cells receptors (fuses similar to endocytosis)
o RNA will go inside T-helper cell then transcribes to make viral DNA
§ Happens in cytoplasm
o Uses a protein to take the HIV strand into the Nucleus through the pores and
destroys the previous DNA
o New virus synthesis
o New virus shedding and death of host cell
o Continues on to next cell
· Zudivudine (AZT) is an antiviral drug that delays the development of AIDS
and slows its progression.
o Acts by interfering with the normal action of reverse transcriptase
Pathogenesis of AIDS
· Treatment can suppress the disease, but the HIV virus can sometimes
continue to transfer (slower though)
· Acute phase
o Minor ‘flu’ with possible nervous system symptoms
· Chronic Phase
o Th cell count is falling
· Crisis Phase
o Long term fever, weight loss, diarrhea, and severe Th cell losses
o Immune system is depleted the likelihood of viruses, tumors, and severe
infections increases
Consequences of Th cell depletion in AIDS Figure 5.27
· Impaired antibody production
o Faulty ADCC and complement-mediated toxicity
§ Increased rate and severity of infection
· Impaired inflammatory response
o Increased rate and severity of infection
· Impaired cellular immunity
o tumor growth
o increased rate and severity of infection
Symptoms of SLE (lupus) Figure 5.28 signs and symptoms
· autoimmune disorder causes widely variable systemic effects
· most typical in African American women
· can happen at any age

Chapter 6 Neoplasia
Neoplasia- abnormally new growth

Tissue Growth Disorders

Adaptive Growth Responses
● reversible changes
○ hypertrophy- fibers get bigger
○ hyperplasia- extra cells
Abnormalities
● Metaplasia- change one cell type to another cell type
● Dysplasia- precancerous; bad growth
○ pleomorphic- multiple shapes and sizes
Developmental growth
● Aplasia- no growth
● Hypolasia- not enough growth
Neoplasia
● irreversible alteration of cells growth pattern
● tissue production beyond the body’s need
○ autonomous growth
● lock of contact inhibition
○ growing indepedently
○ lack of response to ECM
Tumor Terminology
oncology- cancer specialist
Benign- slow growing
Malignant- metastesous; more aggressive/ fast growing
Cancer- new growth
Carcinomas- malignant ectoderm and endodermal derivatives (Bump/mass)
Sarcomas- malignant mesodermal derivatives (fleshy muscle tissue)

Zygote
When sperm & egg meet
cell division/ replication (64-128 cells)

Primary Germ layers

● Ectoderm
○ top layer; skin/nervous systerm