Ig1

“Humoral immunity is a type of immune response that depends on antibodies.” The response begins when a pathogen binds to a B cell. The B cell will engulf the pathogen and display a part of the antigen on its exterior. Once a T cell is exposed to the antigen-presenting B cell, the T cell will release proteins to activate the B cell. Now that the B cell is activated, it will produce antibodies to cause the pathogens to clump together. In the last stage of humoral immunity, phagocytes will engulf and destroy the pathogens.

Patients who underwent this procedure had to remain on immunosuppressive drugs for about 6 months to prevent the recipient’s immune system from destroying the donor cell. One out of seven patients that had this procedure done had a relapse because they stopped taking their immunosuppressant drug during the critical stage of treatment. This treatment has proven successful, but there still remains the concern of tissue rejection and other complication. Nevertheless, this approach still provides encouragement for people suffering with the disease.

Problems can be caused via both types of adaptive immunity because they are frameworks made to help keep up homeostasis inside the body. Cytotoxic T cells are a piece of the cell-intervened kind of versatile resistance. When particular outside cells are identified in the body these cells become activated. Cytotoxic T cells specifically assault attacking antigens inside the body. Antibody-mediated immunity contains B cells that changes into plasma layer that integrates and secretes antibodies that bind to and deactivate particular antigens in the bodies fluids. An organ transplant cells for the most part is perceived in the body as non-self

Active immunizing agents stimulate the body to make its own antibodies and to continue on making them, the

this occurs in a series of steps, the first of which is incorporation of unidentified antigens by APCs in the epidermis and dermis. This process involves binding of the antigens to the MHC on the APC surface and the APC migrates to the lymph nodes. There, the APC binds reversibly and briefly with naïve or resting T cells through interactions between surface molecules located on both cells. Next, the MHC presents the antigen to a T lymphocyte receptor to begin activation of the T lymphocyte. The second signal for T lymphocyte activation is a non-antigen/ cell-cell interaction known as costimulation. If costimulation does not occur, the T lymphocyte will either undergo apoptosis or become unresponsive. Costimulation involves pairing of receptor with ligand on the T cell; these pairs include (LFA)-3 interacting with CD2, B7 interacting with CD28, and ICAM-1 interacting with LFA-1 (Lebwohl, 2003).

Another health problem that treatment with embryonic stem cells can cause is tissue rejection. As is the case with current organ transplantation procedures, embryonic stem cells are harvested from many people all who possess a unique set of genes; therefore, the stem cells are not genetically matched for each patient (Herold 48-49). The difference in genetics causes the body to reject the tissue and the immune system begins to attack the transplanted tissue like it would a virus or bacteria in an attempt to remove the perceived threat. To avoid the implanted tissues being rejected by the body, doctors must prescribe immune suppression drugs that must be taken for the remainder of the patient’s life, even with these drugs the tissue may still be rejected and

The other challenge to transplanting organs is the body’s immune system rejecting the procedure because it is unnatural to it. The body’s immune system is set up to defend the body against any foreign disease-causing bacteria, viruses and or fungi. A procedure like this is alienated by the body at time because it

Many pathological conditions can be treated through the use of allogeneic transplants. An allogeneic transplant is when cells, tissues, or organs from a donor are placed into a recipient that is genetically different. Because the donor and recipient are not identical, it is possible for the graft to reject, which when there is an immune response against the graft. It is also possible for a more serious complication to occur, known as Graft-versus-host disease. Graft-versus-host disease typically occurs in cases of bone marrow or stem cell transplants, but it can also occur in other cases as well. In this condition, immune cells in the grafted tissue recognize the host body cells as foreign, and attack them. Normally, immune cells do not attack their own body cells due to cell proteins called human leukocyte antigens (HLA). Every person has a different HLA pattern, which makes allogeneic transplants more difficult. For a transplant to be successful,

Chronic rejection: slow and progressive, and usually occurs in transplants that survive the initial rejection phases. Scientists are still unclear about the process, and research in this area is very difficult as xenografts rarely survive past the initial acute rejection phases.

A procedure known as transplantation consists of the transfer of cells, tissue or organ from one part of the body to another or from one person to another (National Cancer Institute, no date). Haemopoietic stem cells (HSCs) are unspecialized cells that have the ability to self-renew and the ability to differentiate into the HSCs lineage (Figure 1) for instance as white blood cells (WBCs), red blood cells (RBCs) and platelets. Treatment for a range of haematological disorders usually requires transfusion and transplantation (Knight, 2013). To obtain HSCs for transplantation there are three main sources. They are the bone marrow (BM), peripheral blood stem cells (PBSCs) and umbilical cord blood (UCB) (Smith and Wagner, 2010). A haploidentical donor is another source where the HLA match is not complete and there is a match of one haplotype. HSCs can be transplanted by an autologous, allogeneic and syngeneic donor (Hatzimichael and Tuthill, 2010). HSCs transplantation is carried out to eliminate the condition by myeloablation (prevent immune system attacking/rejecting new graft), to prevent the body being attacked by the new immune system derived from the new HSCs by graft versus host disease (GvHD) and to avoid rejection of the graft by immunosuppression (Buckland, 2017).

Chimerism after a liver transplant most often occurs after a period of 3-4 weeks, with a peak in the first two weeks then declining in the third and fourth weeks [10], hence GVHD predominantly occurs in first few weeks (2-8 weeks). It has been suggested that macrochimerism with > 1% of the circulated donor T-cells in the peripheral blood of recipient confirms donor engraftment, and an increased level of >10% donor CD8+ T/NK cells is indicative of GVHD. Though chimerism is an important investigation, presence of chimerism in absence of clinical symptoms and histological findings is non-specific, making macrochimerism only a diagnostic tool [6, 43-44]. Also the severity and duration of chimerism varies with the evolution of patient and it may be a pre-requisite for acceptance of the graft. So presence of donor HLA in recipient blood within first week post-transplant may not be used to diagnose

The other antigens: Tetanus toxoid, typhoid 0 and H, and streptolysin are proteins, which need T-cells help to activate a B-cell response. For this reason, Dennis's T cells need CD40L to activate his B cells to respond to these protein antigens. He also cannot make antibodies against Streptococcus pyogenes, because the antigenic component of the bacterial capsule is a protein.

Despite the development of these very sensitive anti-HLA screening assays; using that use soluble HLA antigens bound to microplates or beads in the enzyme-linked immunosorbent assay (ELISA) and flow cytometric or Luminex assays and crossmatching techniques, antibody-mediated rejection episodes, confirmed by C4d deposition, still occur without detectable HLA antibodies, suggesting a role for non-HLA antibodies in transplant rejection4 .

As B Cells also work as antigen-presenting cells, the B Cells endocytose the antigens and present it on MHC Class II receptors (without digesting it first) to TH-Cells (Kurosaki et al. 2015), however this promotes proliferation and differentiation of B Cells into plasma cells or memory cells (Kurosaki, Kometani & Ise 2015): see Figure 3. Plasma B Cells produce antibodies (immunoglobulins) that bind to the antigen epitope on that specific bacteria (Gonda 2015) and target it for destruction, attracting phagocytic cells (macrophages) and can activate the complement system (Gonda 2015). As there is a constant stream of billions of antibodies being created against various things, only around 1% of antibodies are specific to that one antigen (Stafford& Johnston 2014). The complement pathway (although considered part of innate immunity, its interconnected with all of the immune response (Sarma & Ward 2011)) has three pathways: classical, alternative, and lectin, which all essentially cleaves inactive zymogene proteins, activating them and converging at the formation of the protein C3 (Sarma & Ward 2011); seen in Figure 2. This ultimately results in the membrane attack complex which drills a 'pore' into the cell membrane of the bacteria and causes osmotic cell lysis (Sarma & Ward 2011). However, C3b coats the bacteria and makes it more 'attractive' to phagocytic cells (known as opsonization),

There are three pathways of allorecognation: direct, indirect, and linked pathways. The difference of direct and indirect pathways is the work of dendritic cells in presenting the donor peptides as foreign antigens. In direct pathway, the dendritic cells migrate directly from the graft into the recipient’s lymph nodes and present the antigen to their own MHC to T cell receptor (TCR). This will excite an anti-donor T-cell allorecognition response and lead to rejection. Both CD4+ and CD8+ are capable for this. Conversely, in indirect pathway, the dendritic cells migrate to the graft, take and process some proteins from the recipient cells and present it on MCH to T cells in lymph nodes. While, linked allorecognation is by using direct transfer of cell membrane from donor dendritic cells to recipient dendritic cells.3,4 (Figure 2)