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I was reading Cellular and Molecular Immunology By Abul K. Abbas, Andrew H. H. Lichtman, Shiv Pillai and stumbled upon the following excerpt $-$
In every individual there are millions of different clones of B-cells,each producing antibody molecules with the same antigen binding site and different in this site from the antibodies produced by other clones.
What are these clones of B-cells, one producing monoclonal antibodies and the other polyclonal antibodies?
When you read further you'll get it. Basically, when the antibody expressed on a B-cell recognizes an antigen, then the B-cell divides and expands its population to produce more antibodies (through plasma cells). This process is called clonal expansion.
Cytokines which are produced by effector T4-helper lymphocytes helps activated B-lymphocytes to proliferate and produce clones.
So, even if limited B-lymphocytes may have an antibody molecule able to bind particular epitope, still many cells are produced with the this specificity. This is clonal expansion (https://i.stack.imgur.com/3OlfJ.jpg">https://bio.libretexts.org/Bookshelves/Microbiology/Book%3A_Microbiology_(Kaiser)/Unit_6%3A_Adaptive_Immunity/13%3A_Humoral_Immunity/13.1%3A_Antibodies_(Immunoglobulins)/13.1E%3A_Clonal_Selection_and_Clonal_Expansion
B cells are a type of cells that produce antibodies. Each B cell produces a different type of antibody. For example, consider the following B cells: C1, C2, and C3, which produce antibodies A1, A2, and A3, respectively. We are dealing with 3 B cell clones, given that they produce 3 different types of antibodies.
Let's say that the B cell C1 happens to produce antibodies (A1) that are specific against the lipopolysaccharide (LPS) of a certain bacteria. When this bacteria enters the body, C1 will detect its presence and become activated. Two things happen when a B cell becomes activated: (1) differentiation, and (2) proliferation. Therefore, from the B cell clone C1 many more B cells will be produced through cell division, and all of these cells will produce antibodies A1 with the same affinity towards LPS. This would be a monoclonal antibody response, given that only antibodies from one B cell clone are produced.
If B cell C2 also produces antibodies (A2) with affinity for LPS, then upon bacterial infection C2 would become activated, proliferate, and differentiate. Given that antibodies (A1 and A2) from two different B cell clones (C1 and C2) are produced, this is a polyclonal antibody response.
Hope this helps!
Clonal anergy , defined as the presence of antigen-specific B cells in an unresponsive state, can be achieved by a number of mechanisms. Some involve modulation of the signaling of the B cell itself, while others alter the ability of these B cells to solicit and respond to T cell help. Still other mechanisms alter the location of anergic B cells in the lymphoid system and their lifespan. Why are so many tolerance mechanisms employed when it would be simpler to delete any lymphocyte which showed traces of self reactivity? Several explanations have been put forward to answer this question, most cogently by Goodnow. First, not all self antigens will be present in bone marrow when the B cells are developing and sensitive to tolerance induction. Second, if all B cells which show any degree of binding to self antigens were to be deleted, it is questionable that the lymphoid system could generate a sufficient number of cells to counter the infectious agents animals are exposed to. That is, anergy may be a means by which the immune system is able to silence potentially harmful B cell clones and yet have B cells survive long enough to be exported to the peripheral lymphoid organs. In these locations it is possible that the anergic B cells may encounter a foreign antigen to which they have a higher affinity than that with which they recognize the self antigen. If this were the case, then the anergic B cell could be activated and participate in a protective immune response. The anergic B cells would quickly die, however, if no such foreign antigen existed at the time it reached the periphery. This may also account for the reversibility of B cell anergy.
Monoclonal B-cell lymphocytosis, or MBL for short, is an asymptomatic condition characterized by the presence of a circulating small clonal B-lymphocyte population in persons who do not have chronic lymphocytic leukemia (CLL), other B-cell lymphoproliferative disorder, or underlying conditions such as infectious or autoimmune disorders .
Despite the fact that the majority of subjects diagnosed with MBL does not develop CLL [2,3], a large population-based cancer study suggests that MBL may precedes CLL by several years in some cases . Efforts are on-going to identify at molecular level patients with MBL at higher risk of developing CLL in order to design intervention approaches able to delay or prevent CLL progression.
T-cells and cell-mediated immunity
T-cells respond to specific antigens. When a pathogen first infect the body, each individual antigen stimulates a single t-cell. This divides to form a clone, in the same way that B-cells do. Som of the activated t-cells become memory cells and persist in the body, ready to mount a secondary response if the pathogen attaks again. The others, however, do not produce antibodies. They develop further to become either helper T-cells, Killer T-cells or suppressor T-cells.
The surface of each T cell also displays thousands of identical T cell receptors (TCRs). The TCR binds a bimolecular complex displayed at the surface of some other cell called an antigen-presenting cell (APC). This complex consists of:
Most of the T cells in the body belong to one of two subsets. These are distinguished by the presence on their surface of one or the other of two glycoproteins designated:
CD4 - CD4 + T cells bind an epitope consisting of an antigen fragment lying in the groove of a class II histocompatibility molecule. CD4 + T cells are essential for both the cell-mediated and antibody-mediated branches of the immune system:
These CD4 + cells bind to antigen presented by antigen-presenting cells (APCs) like phagocytic macrophages and dendritic cells. The T cells then release lymphokines that attract other cells to the area. The result is inflammation: the accumulation of cells and molecules that attempt to wall off and destroy the antigenic material (an abscess is one example, the rash following exposure to poison ivy is another).
These CD4 + cells, called helper T cells, bind to antigen presented by B cells (as shown above). The result is the development of clones of plasma cells secreting antibodies against the antigenic material.
CD8 - The best understood CD8 + T cells are cytotoxic T lymphocytes (CTLs). They secrete molecules that destroy the cell to which they have bound. This is a very useful function if the target cell is infected with a virus because the cell is usually destroyed before it can release a fresh crop of viruses able to infect other cells.
Every time you get a virus infection, say influenza (flu), the virus invades certain cells of your body (in this case cells of the respiratory passages). Once inside, the virus subverts the metabolism of the cell to make more virus. This involves synthesizing a number of different macromolecules encoded by the viral genome.
In due course, these are assembled into a fresh crop of virus particles that leave the cell (often killing it in the process) and spread to new target cells.
Except while in transit from their old homes to their new, the viruses work inside of your cells safe from any antibodies that might be present in blood, lymph, and secretions.
But early in the process, infected cells display fragments of the viral proteins in their surface class I molecules. CTLs specific for that antigen will be able to bind to the infected cell and often will be able to destroy it before it can release a fresh crop of viruses.
In general, the role of the CD8 + T cells is to monitor all the cells of the body, ready to destroy any that express foreign antigen fragments in their class I molecules.
Which of these molecules is present determines what types of cells the T cell can bind to.
Why Human Cloning is Difficult?
- Reproductive human cloning faces a lot of technical difficulties.
- The success rate of SCNT is very low.
- During the cloning of Dolly, the success rate was (29) embryos per (277) tries.
- In macaque monkeys, out of (100) cloned embryos implanted in (50) females, none survived.
- Reproductive cloning using SCNT is considered harmful as nuclear damage is involved while enucleating and inserting the donor nucleus.
- The cloned embryos rarely make the full term of gestation and may get birth defects.
- Maintaining human embryo viability after SCNT is challenging, and embryos die at an early stage.
- Some scientists argue that current technological advances are not enough to clone primates and humans.
Two 100-μl samples of thawed blood were placed in two tubes for staining. They were washed three times with the use of Sorvall cell washers. Then 10 μl of rabbit immunoglobulin was added and incubated at 37°C for 30 minutes, followed by 10 μl of an isotypic cocktail (consisting of fluorescein isothiocyanate–conjugated IgG, phycoerythrin-conjugated IgG, peridinin–chlorophyll–protein cyanine 5.5–conjugated anti-CD19 antibodies, phycoerythrin–cyanine 7–conjugated IgG, allophycocyanin-conjugated IgG, and allophycocyanin H7–conjugated anti-CD45 antibodies), which was added to one tube the second tube was stained with the custom conjugated six-color antibodies cocktail (consisting of fluorescein isothiocyanate–conjugated anti-CD5, phycoerythrin-conjugated anti-lambda, peridinin–chlorophyll–protein cyanine 5.5–conjugated anti-CD19 antibodies, phycoerythrin–cyanine 7–conjugated CD10, allophycocyanin-conjugated anti-kappa, and allophycocyanin H7–conjugated anti-CD45 antibodies) and incubated for 20 minutes. All antibodies were obtained from BD Biosciences. After this procedure, 1 ml of red-cell lyse buffer was added to each tube and incubated for 10 minutes and then washed with Sorvall cell washer. Cells were then resuspended in 350 μl of phosphate-buffered saline and acquired with the use of FACSCanto flow cytometry daily quality control and assurance were carried out with the use of seven-color setup beads (BD Biosciences).
Types of B-Cell Lymphomas
When your doctor talks to you about your B-cell lymphoma, they'll explain which type you have. The most common type of non-Hodgkin's lymphoma is called diffuse large B-cell lymphoma (DLBCL).
Other types of B-cell non-Hodgkin's lymphoma include:
- Follicular lymphoma -- a slow-growing form that mainly affects older adults
- Chronic lymphocytic leukemia/small lymphocytic leukemia (CLL/SLL) -- slow growing types that are closely related
- Mantle cell lymphoma -- a fast-growing lymphoma
- Marginal zone lymphoma -- a type that features small cells that grow slowly
- Burkitt lymphoma -- a rare disease that grows quickly
- Lymphoplasmacytic lymphoma (Waldenstrom macroglobulinemia) -- a rare and slow-growing lymphoma
- Primary mediastinal large B-cell lymphoma -- a rare type that mainly affects young adults, and is more common in women
A clone refers to hardware or software.
With hardware, a clone is a derogatory term that means "close but not quite" or an outright "copy" of lesser quality. Hardware clones are often made by stealing original designs or through reverse engineering.
In any case, the result is often of lesser quality, as the cloner markets the product as the original - right down to the packaging - to ride its popularity through customer deception. This is hardware piracy.
An early example of cloning was the first IBM PC, where rival companies like Dell and Compaq began selling comparable versions at lower costs, which also helped lower computer costs.
Similarly, software clones are created to ride the popularity of a product's original marketing. For example, Zynga's social farming game, FarmVille, was popularized on Facebook and quickly cloned by other developers that employed similar features and mechanics but altered visual aspects just enough to avoid lawsuits.
Games in the same genre can even be considered clones of earlier games because of similar gameplay mechanics and visuals.
B cells mature in the bone marrow. Once activated, B cells have binding sites that are specific to a pathogen. When the antigen is present, it binds to the receptor on the B cell. This triggers the B cell to grow and clone itself. The clones become either plasma cells or memory cells. The plasma cells generate massive amounts of antibodies and release them into the body. The antibody binds to the antigen signaling the cells of the internal defenses to come and kill the pathogen. The plasma cells die within a few days.
Memory cells do not secrete antibodies. Instead, memory cells retain the antibody so that it can be used anytime the antigen is re-encountered. Memory cells are important because they help the body mount a faster and stronger attack the next time the antigen invades. This is called immunological memory. During this secondary immune response, antibodies exist in the body for a much longer period of time--up to months--and antibodies bind more effectively to the antigen.
B cells link the innate and adaptive arms of immune response by their ability to respond rapidly to damage-associated molecular patterns and antigenic stimuli, and also form long-lived serologic memory. B cells perform diverse functions, such as antibody secretion, cytokine production, antigen presentation, and lymphoid architecture organization, that intersect with both innate (such as DCs) and adaptive T-cell roles in shaping the outcome of the immune response toward immunity or tolerance ( Figures 6 and and7). 7 ). Disruption of B-cell tolerance by cell-intrinsic (BCR signaling) or cell-extrinsic (BAFF, T-cell help) defects, dysregulated BAFF levels, and impaired regulatory functions contribute to pathogenesis of autoimmunity. Depleting B cells could therefore potentially re-establish B-cell tolerance by purging autoreactive clones, eliminate pathogenic antibody-producing B cells, and interrupt cellular functions of B cells that enhance pathogenic T cell activation. However, nonselective pan-depletion of B cells can also remove the beneficial Bregs, increase BAFF levels, and potentially worsen disease. Instead, targeting B cells to correct specific defects or remove pathogenic B cells while sparing others would prevent undesired immune activation or immune deficiency. Future studies aimed at disease-specific understanding of how pathogenic B cells arise could facilitate not only the development of novel selective therapies but also the optimal use of existing therapies, such as rituximab and belimumab, for best outcomes.