B) Remove aging and damaged blood cells

Explanation: The spleen's major function is to remove aging and damaged blood cells or particles from the circulation and to initiate adaptive immune responses to blood-borne antigens.

B) To present antigens to CD4+ helper T cells

Explanation: MHC Class II molecules present antigens to CD4+ helper T cells, which is crucial for initiating the helper T cell response.

C) Bone marrow

Explanation: Bone marrow is a primary lymphoid organ where partial maturation of B lymphocytes occurs.

B) Chemokines

Explanation: Chemokines present in the paracortex attract dendritic cells so they can present antigens to T helper cells.

C) More rapid and effective with each subsequent exposure for adaptive

Explanation: Adaptive immunity becomes more rapid and effective with each subsequent exposure due to the presence of memory cells.

B) Activation, proliferation, and differentiation of lymphocytes

Explanation: Clonal selection involves the activation, proliferation, and differentiation of lymphocytes that recognize a specific antigen, leading to the formation of plasma cells, effector cells, and memory cells.

C) Helper T cells

Explanation: Helper T cells produce cytokines, which are crucial for regulating immune responses.

D) Corticomedullary junctions

Explanation: Thymocytes enter the thymus via blood vessels located in the corticomedullary junctions, which is the initial point of entry before they migrate to other regions of the thymus.

B) Inhibits activation of macrophages and dendritic cells

Explanation: IL-10 is a cytokine that inhibits the activation of macrophages and dendritic cells, acting as a negative feedback regulator in the immune response.

A) Pain, redness, heat, swelling, and loss of function

Explanation: The cardinal signs of inflammation are pain (dolor), redness (rubor), heat (calor), swelling (tumor), and loss of function (functio laesa), which can be explained by increased blood flow, elevated cellular metabolism, vasodilation, release of soluble mediators, and extravasation of fluids.

B) Production of cytokines TNF and IL-1

Explanation: The first step in leukocyte recruitment into tissues is the production of cytokines TNF and IL-1 by activated macrophages, mast cells, and other sentinel cells at the site of infection.

B) Paracortex (T cell zone)

Explanation: Migratory dendritic cells move toward the paracortex (T cell zone) through the afferent lymphatics to present antigens to T helper cells.

B) To present antigens to CD4+ helper T-cells

Explanation: Activated B-cells present antigens to CD4+ helper T-cells, facilitating T-cell and B-cell interactions crucial for humoral immune responses.

B) To present antigens to CD8+ cytotoxic T-cells

Explanation: MHC Class I molecules present antigens to CD8+ cytotoxic T-cells, which is crucial for the immune response against intracellular infections.

B) Death of the infected cell

Explanation: When CD8+ cytotoxic T-cells recognize an antigen presented by MHC Class I molecules, it leads to the death of the infected cell.

E) CD19

Explanation: CD19 is a characteristic marker of B cells, not T cells.

C) Provide long-term immunity

Explanation: Memory lymphocytes are responsible for providing long-term immunity by remembering past infections.

C) Antigen presentation to CD4+ effector T-cells in the effector phase of cell-mediated immune responses

Explanation: Macrophages present antigens to CD4+ effector T-cells in the effector phase of cell-mediated immune responses.

B) Cytokine counteracts or inhibits the actions of another cytokine

Explanation: Antagonism refers to a cytokine counteracting or inhibiting the actions of another cytokine, thereby having opposing effects.

B) FasL

Explanation: FasL expressed on cytotoxic T cells interacts with Fas on host cells, leading to the sequential activation of proteolytic enzymes called caspases, which cause cell death within hours.

B) Monocytes, dendritic cells, and B cells

Explanation: Professional antigen-presenting cells include monocytes, dendritic cells, and B cells, which are essential for presenting antigens to T-cells.

B) Spleen

Explanation: B cells remain in the bone marrow initially and continue their development in the spleen.

B) T cells

Explanation: T cells mature in the thymus, whereas B cells mature in the bone marrow.

C) Once or twice a day

Explanation: An individual lymphocyte completes a circuit from the blood to the tissues and lymph nodes and back again once or twice a day.

B) They recognize pathogen-associated molecular patterns

Explanation: PRRs (Pattern Recognition Receptors) recognize pathogen-associated molecular patterns, inducing the inflammatory response and the secretion of chemokines, cytokines, IFNs, and other antimicrobials.

B) CRP

Explanation: CRP (C-reactive protein) is an opsonin that enhances phagocytosis by marking pathogens for destruction by immune cells.

A) TNF, IL-1, IL-6, and chemokines

Explanation: Sentinel cells produce cytokines such as TNF, IL-1, IL-6, and chemokines at the site of infection, which increase local delivery of cells and attract WBCs to the site of infection.

C) Spleen

Explanation: Transitional B cells leave the bone marrow and complete their maturation in the spleen, where they acquire surface IgD in addition to IgM.

A) To bind to MHC molecules

Explanation: Mature T cells express either CD4+ or CD8+ to bind to MHC molecules, which is crucial for their role in the immune response.

B) Suppress the immune response

Explanation: T regulatory cells suppress the immune response through mechanisms such as cytokine deprivation, secretion of inhibitory cytokines, inhibition of antigen-presenting cells, and cytotoxicity.

C) Antigen-presenting cells like macrophages, dendritic cells, and activated B cells

Explanation: MHC Class II molecules are expressed on antigen-presenting cells such as macrophages, dendritic cells, and activated B cells.

C) Removes aged and damaged RBCs

Explanation: The spleen removes aged and damaged red blood cells and is also a site for the complete maturation of B cells.

B) Minutes to hours

Explanation: Innate immunity responds quickly, within minutes to hours, providing an immediate defense against infection.

B) High-affinity receptors for certain opsonins

Explanation: Phagocytosis requires that phagocytes possess high-affinity receptors for certain opsonins, such as antibody molecules, complement proteins, and plasma lectins.

D) Interferon gamma (IFNγ)

Explanation: The three classes of microbicidal molecules are reactive oxygen species (ROS), nitric oxide (NO), and lysosomal enzymes. Interferon gamma (IFNγ) is not a class of microbicidal molecules.

B) To bring leukocytes and plasma proteins to infection sites

Explanation: Inflammation is the process by which leukocytes and circulating plasma proteins are brought into sites of infection and activated to destroy and eliminate the offending agents.

C) IL-2

Explanation: T-cells respond by producing and expressing IL-2 receptors, leading to an autocrine pathway of cell proliferation.

C) SOCS proteins

Explanation: Suppressors of cytokine signaling (SOCS) proteins inhibit JAK-STAT signaling pathways linked to cytokine receptors, thereby regulating the immune response.

B) Enhances phagocytosis and forms the Membrane Attack Complex (MAC)

Explanation: The complement system enhances phagocytosis through opsonization and forms the Membrane Attack Complex (MAC) to lyse pathogens.

B) Increases plasma viscosity and erythrocyte sedimentation rate (ESR)

Explanation: C-reactive protein (CRP) is an acute phase protein that increases plasma viscosity and consequently increases the erythrocyte sedimentation rate (ESR), serving as a marker for inflammation.

B) They produce polarizing cytokines

Explanation: PRRs on APCs detect pathogen-associated molecular patterns (PAMPs) from pathogens, influencing the production of specific polarizing cytokines that guide the differentiation of naive T cells into specific T helper cell subsets.

E) PALT

Explanation: The types of mucosa-associated lymphoid tissues (MALT) include NALT (Nasal), BALT (Bronchus), SALT (Skin), and GALT (Gut). PALT is not a recognized type of MALT.

B) Produce antibodies

Explanation: Effector B cells, also known as plasma cells, are responsible for producing antibodies.

C) Natural barriers (skin, mucous membranes)

Explanation: Innate immunity includes natural barriers such as skin and mucous membranes, as well as phagocytes, NK cells, and soluble mediators like cytokines and complement.

C) Paracortical area

Explanation: T cells are primarily located in the paracortical area of the lymph nodes.

C) Thymus

Explanation: The thymus is a primary lymphoid tissue where T cells mature before entering the circulation and migrating to secondary lymphoid organs.

C) Commitment of hematopoietic precursors to the T cell lineage

Explanation: During the early thymocyte development phase, hematopoietic precursors commit to the T cell lineage, initiate T cell receptor gene rearrangements, and expand cells that have successfully undergone gene rearrangement.

B) It prevents the spread of infectious viruses

Explanation: Apoptosis induced by cytotoxic T cells does not result in the release of cell contents, thereby preventing an inflammatory response and the spread of infectious viruses to other cells.

C) Block infections and eliminate extracellular microbes

Explanation: Humoral immunity, mediated by B lymphocytes and antibodies, primarily functions to block infections and eliminate extracellular microbes.

A) Neutrophils

Explanation: Neutrophils increase during acute bacterial infections, playing a crucial role in the body's immediate response to bacterial pathogens.

D) Highly diverse; adapts to improve during the course of immune response

Explanation: Adaptive immunity is characterized by its high diversity and ability to adapt and improve its response during the course of an immune response.

E) 50%

Explanation: After 30 minutes in circulation, 50% of the mature naive lymphocytes produced by the thymus and bone marrow travel directly to the spleen.

C) Thymus

Explanation: T cells mature in the thymus before entering the circulation and migrating to secondary lymphoid organs.

C) Tissue-resident macrophages, dendritic cells, kupffer cells, and mast cells

Explanation: Sentinel cells, such as tissue-resident macrophages, dendritic cells, kupffer cells, and mast cells, are already present in the injured area and initiate inflammation.

B) Antigen recognition

Explanation: The first step in the activation of T-lymphocytes is the recognition of major histocompatibility complex-associated peptide antigens displayed on antigen-presenting cells (APCs).

C) TGF-β

Explanation: Transforming Growth Factor β (TGF-β) is an anti-inflammatory cytokine that inhibits inflammation.

C) IgM

Explanation: The first antibody produced by an immature B cell is of the IgM class, marking the initial stage of antibody production in B cell development.

B) Promotes differentiation of TH2 cells

Explanation: IL-17E (IL-25) promotes the differentiation of the anti-inflammatory T helper 2 (TH2) cell subclass while suppressing T17 cell responses.

B) Recruits immune cells to the inflammation site

Explanation: Serum amyloid A is an acute phase protein that recruits immune cells to the site of inflammation and can rise a thousand-fold in blood concentration during inflammation.

D) TFH

Explanation: TFH (Follicular helper T cells) are primarily involved in activating B cells and are found in the follicles of lymph nodes.

C) Cervical lymph nodes

Explanation: The initiation of the adaptive immune response occurs in lymph nodes such as cervical, axillary, and inguinal nodes, where antigens are captured and recognized by B and T cells.

C) To instruct B-cells to produce antibodies

Explanation: CD4+ helper T-cells play a crucial role in the immune response by instructing B-cells to produce antibodies, which help in opsonizing pathogens.

C) 5%

Explanation: Only 5% of mature lymphocytes are found in the circulation, where they constitute 20-35% of all white blood cells (WBCs).

D) Cells of the innate immune system

Explanation: Cells of the innate immune system use pattern recognition receptors to recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs).

C) The T cell will turn off

Explanation: If a T cell receives signal 1 (TCR signaling) but not signal 2 (costimulatory interaction), the T cell will turn off.

B) By releasing granules containing perforin and granzymes

Explanation: Cytotoxic T cells induce apoptosis in target cells by releasing granules containing perforin, which forms pores in the target cell membrane, and granzymes, which pass into the target cell to induce cell death.

B) Mimic the reactive specificity of the original lymphocytes

Explanation: Memory cells mimic the reactive specificity of the original lymphocytes that responded to the antigen, allowing for a more rapid and effective response upon subsequent exposures.

C) Local lymph node

Explanation: Antigen recognition mainly occurs at the local lymph node, which induces the activation, proliferation, and differentiation of the responsive lymphocytes.

B) They undergo apoptosis

Explanation: During positive selection, T cells that do not bind to MHC molecules undergo apoptosis, ensuring that only T cells capable of recognizing MHC molecules survive.

B) Natural antagonist of IL-1

Explanation: IL-1 receptor antagonist (IL-1RA) is a natural antagonist of IL-1, produced by macrophages to regulate the immune response.

B) They undergo apoptosis

Explanation: During negative selection, T cells that bind strongly to MHC and self-antigens undergo apoptosis to ensure self-tolerance and prevent autoimmune responses.

B) Sequential activation of cytokines in response to a stimulus

Explanation: Cascade induction involves the sequential activation of cytokines in response to a stimulus, amplifying and coordinating immune responses.

B) White pulp

Explanation: The white pulp of the spleen is rich in lymphocytes and includes the T cell zone (Periarteriolar lymphoid sheath/PALS) and the B cell zone (follicles).

B) Secreting immunoglobulins

Explanation: Plasma cells are specialized for the synthesis and secretion of immunoglobulins, which are crucial for the adaptive immune response.

B) TNF, IL-1, IL-6

Explanation: TNF, IL-1, and IL-6 produced at inflammatory sites enter the blood and work with CSF to enhance the production of leukocytes, especially neutrophils, from bone marrow progenitors.

B) They are fused with lysosomes to form phagolysosomes

Explanation: Once internalized into phagosomes, microbes are fused with lysosomes to form phagolysosomes, where they are killed by microbicidal agents.

C) Anti-viral agent in some forms of viral hepatitis

Explanation: Interferon α (IFNα) is used clinically as an anti-viral agent in some forms of viral hepatitis and also for the treatment of some tumors.

B) Extracellular bacteria and pathogens in cellular vesicles

Explanation: MHC Class II molecules primarily present antigens from extracellular bacteria and pathogens that replicate in cellular vesicles.

C) Antibodies

Explanation: Antibodies are part of adaptive immunity, whereas innate immunity includes components like phagocytes, NK cells, natural barriers, and pattern recognition molecules.

C) Dendritic cells, Langerhans cells, Macrophages, B-cells

Explanation: Classical APCs include dendritic cells, Langerhans cells, macrophages, and B-cells.

C) They internalize pathogens, digest them into peptides, and present these peptides on their membrane surfaces via MHC class II molecules

Explanation: Upon encountering pathogens, APCs internalize the pathogens, digest them into peptides, and present these peptide antigens on their membrane surfaces via MHC class II molecules.

B) IL-1, IL-6, TNF-α

Explanation: The acute phase response is stimulated by pro-inflammatory cytokines such as IL-1, IL-6, and TNF-α, which are produced by innate immune cells.

C) It migrates to the T-cell area of the lymph node

Explanation: Upon recognizing a microbe, a dendritic cell becomes mature and migrates to the T-cell area of the lymph node to present antigens to CD4+ T cells.

D) They encounter blood-borne antigens

Explanation: Lymph nodes encounter antigens from the lymphatic system, not blood-borne pathogens.

B) It activates leukocytes to make attachment firmer

Explanation: Chemokine IL-8 activates leukocytes to make their attachment firmer, allowing them to extravasate through the endothelium and migrate towards the source of chemotactic factors.

C) In the follicles and lymph nodes

Explanation: Resting B-cells reside in the follicles and lymph nodes and gain the capacity to activate T-cells after binding to an antigen through their B-cell receptor.

C) Dendritic cells, macrophages, and B-cells

Explanation: MHC Class II molecules are expressed on dendritic cells, macrophages, and B-cells, and they present antigens to CD4+ helper T-cells.

C) By transporters associated with antigen-processing (TAP)

Explanation: Degraded viral proteins are transported into the ER by specific transporter proteins called transporters associated with antigen-processing (TAP) for MHC Class I presentation.

B) They secrete histamine and prostaglandins

Explanation: Mast cells respond to PAMPs and DAMPs by secreting histamine and prostaglandins, which cause vasodilation and increased capillary permeability, enhancing blood flow and movement of plasma proteins.

B) Kill infected target cells and activate macrophages

Explanation: CD8+ cytotoxic T-cells are responsible for killing infected target cells and activating macrophages.

C) Leukocytes attach on the surface of blood vessels

Explanation: During the selectin-mediated rolling of leukocytes, leukocytes attach on the surface of blood vessels through adhesion molecules, initiating the process of leukocyte recruitment.

B) Delivers immune cells and nutrients to the injured area

Explanation: Increased blood flow during an inflammatory response delivers immune cells and nutrients to the injured area, aiding in the immune response.

A) TH1

Explanation: TH1 cells primarily target macrophages, enhancing their phagocytic and antimicrobial activities.

C) Only when antigens are bound to MHC molecules

Explanation: T cells recognize antigens only when they are processed and presented in the groove of MHC molecules on the surface of antigen-presenting cells.

D) Antibody binding

Explanation: The three signals required for naive T-cell activation are TCR signaling, costimulatory interaction, and cytokine signaling. Antibody binding is not one of these signals.

C) Kill infected target cells

Explanation: Effector CD8+ cytotoxic T lymphocytes respond by killing infected target cells and activating macrophages.

C) Have an enhanced ability to react against antigens

Explanation: Memory T cells are long-lived and have an enhanced ability to react against antigens, providing a quicker and more effective response upon re-exposure to the same antigen.

C) Regulate interaction routes

Explanation: Chemokines regulate the interaction routes and direct lymphocytes to their respective zones.

B) To activate macrophages to kill pathogens in vesicular compartments

Explanation: CD4+ helper T-cells assist in the destruction of parasites in vesicular compartments by activating macrophages that harbor pathogens to kill them.

B) To generate T cells that express a diverse array of receptor specificities

Explanation: The main purpose of T cell development is to generate a large population of T cells that express a diverse array of receptor specificities that interact with self-MHC/peptide complexes but do not react against them.

C) Their strategic location at common sites of entry of microbes and high expression of peptide MHC complexes

Explanation: Dendritic cells are strategically located at common sites of entry of microbes and express high levels of peptide MHC complexes, costimulators, and cytokines, making them the most efficient APCs for initiating primary T-cell responses.

B) The adaptive response produces a greater magnitude secondary response

Explanation: Upon repeated exposure to the same antigen, the adaptive immune response produces a greater magnitude secondary response that peaks earlier compared to the primary response.

B) Elevated levels of acute phase proteins

Explanation: The induction of fever during the acute phase response is caused by the hypothalamus responding to elevated levels of acute phase proteins, with TNF and IL-1 acting on the hypothalamus to increase the synthesis of prostaglandins.

B) By interacting with MHC class II molecules

Explanation: T regulatory cells can interact directly with MHC class II expressing antigen-presenting cells and inhibit their maturation, preventing them from presenting antigens effectively.

E) Increased blood pressure

Explanation: The hallmark characteristics of a localized inflammatory response include redness, pain, heat, swelling, and loss of function, but not increased blood pressure.

B) IL-10 and TGF-β

Explanation: T regulatory cells secrete regulatory cytokines IL-10 and TGF-β, which bind to receptors on activated T cells and reduce their signal activity, thereby inhibiting T cell activation.