For an experiment, the hapten DNP was conjugated with the carrier protein BSA or with the carrier protein OVA. A set of mice were primed with either DNP‐BSA conjugate or with OVA which was not conjugated to DNP. The following experiments were then performed. A. X‐ray irradiated syngeneic mice were injected with spleen cells from both DNP‐BSA–primed mice and OVA‐primed mice and then challenged with DNP‐OVA conjugate. B. X‐ray irradiated syngeneic mice were injected with T‐cell depleted spleen cells from DNP‐BSA–primed mice and spleen cells from OVA‐primed mice and then challenged with DNP‐OVA conjugate. C. X‐ray irradiated syngeneic mice were injected with spleen cells from DNP‐BSA–primed mice and T‐cell depleted spleen cells from OVA‐primed‐mice and then challenged with DNP‐OVA conjugate. Which one of the following options of mice will generate secondary anti‐hapten response to DNP?
The mice in experiments A and B
Understanding Hapten-Carrier Conjugates and Immune Response
In immunology, a hapten is a small molecule that can bind to a specific antibody but cannot by itself elicit an adaptive immune response. To become immunogenic (capable of eliciting an immune response), a hapten must be conjugated to a larger molecule, typically a protein, known as a carrier protein. The resulting hapten-carrier conjugate can then induce antibody production against both the hapten and the carrier protein.
A secondary immune response is a faster and stronger response that occurs upon subsequent exposure to an antigen, due to the presence of memory cells generated during the primary response. For a strong antibody response to a hapten conjugated to a carrier, helper T cells specific to the carrier protein are usually required. These helper T cells provide signals that help B cells (which recognize the hapten part) differentiate into antibody-producing plasma cells and memory cells.
Priming and Memory Cell Generation
In this experiment, mice were primed with either DNP-BSA or OVA:
- Mice primed with DNP‐BSA developed an immune response and generated memory cells specific for both DNP (hapten) and BSA (carrier). This includes memory B cells specific for DNP and memory T cells specific for BSA.
- Mice primed with OVA developed an immune response and generated memory cells specific for OVA (carrier). This includes memory T cells specific for OVA.
All subsequent experiments involve transferring spleen cells containing these memory populations into irradiated syngeneic mice and then challenging these recipient mice with DNP‐OVA. To generate a secondary anti-hapten (anti-DNP) response upon challenge with DNP-OVA, memory B cells specific for DNP must receive help from memory T cells specific for the carrier used in the challenge, which is OVA.
Analyzing Experiment A
In experiment A:
- Mice received spleen cells from DNP‐BSA–primed mice (source of anti-DNP memory B cells and anti-BSA memory T cells).
- Mice received spleen cells from OVA‐primed mice (source of anti-OVA memory T cells).
- Mice were challenged with DNP‐OVA.
Here, memory B cells specific for DNP are provided by the DNP-BSA-primed mice. Helper T cells specific for the challenging carrier, OVA, are provided by the OVA-primed mice. Since both components (anti-DNP memory B cells and anti-OVA memory T cells) required for a secondary anti-DNP response are present, a secondary anti-hapten response to DNP is expected.
Analyzing Experiment B
In experiment B:
- Mice received T‐cell depleted spleen cells from DNP‐BSA–primed mice (primary source of anti-DNP memory B cells, but few or no anti-BSA memory T cells).
- Mice received spleen cells from OVA‐primed mice (source of anti-OVA memory T cells).
- Mice were challenged with DNP‐OVA.
Even though the cells from DNP-BSA-primed mice are T-cell depleted, they still contain memory B cells specific for DNP. The essential helper T cells specific for the challenging carrier (OVA) are provided by the spleen cells from the OVA-primed mice. Therefore, the necessary components are present for a secondary anti-hapten response to DNP.
Analyzing Experiment C
In experiment C:
- Mice received spleen cells from DNP‐BSA–primed mice (source of anti-DNP memory B cells and anti-BSA memory T cells).
- Mice received T‐cell depleted spleen cells from OVA‐primed mice (primary source of anti-OVA memory B cells, but few or no anti-OVA memory T cells).
- Mice were challenged with DNP‐OVA.
Memory B cells specific for DNP are present. However, the helper T cells specific for the challenging carrier (OVA) are largely absent because the spleen cells from the OVA-primed mice were T-cell depleted. The T cells present from the DNP-BSA-primed mice are specific for BSA, not OVA, and thus cannot provide effective help for the anti-DNP response when challenged with DNP-OVA. Therefore, a strong secondary anti-hapten response is not expected.
Conclusion on Secondary Anti-Hapten Response
Based on the analysis of each experiment and the requirement for carrier-specific T cell help for a secondary anti-hapten response:
- Experiment A provides both anti-DNP memory B cells and anti-OVA memory T cells, enabling a secondary response.
- Experiment B provides anti-DNP memory B cells and anti-OVA memory T cells, enabling a secondary response.
- Experiment C provides anti-DNP memory B cells but lacks sufficient anti-OVA memory T cells, limiting a strong secondary response.
Thus, the mice in experiments A and B are expected to generate a secondary anti-hapten response to DNP when challenged with DNP-OVA.
Important Questions from Cellular communication
In a neuron, proteins and membranes are primarily synthesized in the cell body. These materials must be transported down the axon to the synaptic region using microtubules in an anterograde fashion. Such axonal transport is directed by
Acetylcholine is a potent neurotransmitter, which is released from the neurons. After release they diffuse across the synaptic cleft and combine with nicotinic acetylcholine receptor molecules in the membrane of the postsynaptic cell. The interaction of acetylcholine with the nicotinic acetylcholine receptor produces large transient increase in the permeability of the membrane to specialized ions resulting in signal transduction for nerve impulse. Acetylcholine receptor is a
Column X represents the type of junctions and column Y represents the proteins associated with the junctions.
Column X
Column Y
A.
Anchoring junction
i.
Claudins
B.
Occluding junction
ii.
Delta-Notch
C.
Channel-forming junction
iii.
Desmoglein
D.
Signal-relaying junction
iv.
Connexin
Which one of the following options is a correct match between terms of Columns X and Y?
Bacteria employ various mechanisms to invade or enter host cells, which are either phagocytic or non-phagocytic in nature. Given below are some of the mechanisms which are generally used for carrying out this process.
A. Some bacteria express a protein called invasin that is recognized by host-cell β1 integrins.
B. Actin polymerization along with assembly of clathrin coat results in the internalization of bacteria by zipper mechanism.
C. Some bacteria, including Salmonella enterica, use trigger mechanism to inject a set of effector molecules in the cytosol through type III secretion system.
D. Some bacteria attach to host cell surface receptors inducing local elevation of Ca2+ in cell cytosol, leading to the fusion of lysosomes with bacteria containing plasma membrane vesicles.
Which one of the following represents the combination of correct mechanisms for invading non-phagocytic cells?
In C. elegans, PAR proteins segregate at the cell cortex in the zygote to establish cell polarity. This is dependent on the regulation of the cortical actin cytoskeleton by RhoA. An investigator sought to directly inhibit actin polymerization to analyze the impact of this inhibition on PAR protein localization. Which one of the following chemicals would be the most suitable?
