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Related Concept Videos

Lymphoid Cells and Tissues01:18

Lymphoid Cells and Tissues

Lymphoid cells and tissues are integral to the immune system, which is crucial in maintaining our body's defense against harmful pathogens. They form the building blocks of lymphoid organs, which include the spleen, thymus, and lymph nodes.
Lymphoid cells consist of various types of immune system cells. These include B and T lymphocytes, which are responsible for producing antibodies and killing infected cells, respectively. Dendritic cells act as messengers between the innate and adaptive...
Secondary Lymphoid Organs01:15

Secondary Lymphoid Organs

Secondary organs, including lymph nodes, the spleen, and mucosa-associated lymphoid tissue (MALT), work harmoniously to protect us from disease and infection.
The spleen is a vital organ in the lymphatic system, nestled in the upper left side of the abdomen. It is composed of two primary regions: the red pulp and the white pulp, each having distinct functions. The red pulp performs a significant role in blood filtration. It efficiently purges the blood of old or damaged red blood cells and...
Primary Lymphoid Organs01:16

Primary Lymphoid Organs

Primary lymphoid organs are pivotal in the formation, development, and maturation of lymphocytes, the white blood cells that serve as the backbone of our immune system. This crucial function underscores their fundamental role in maintaining our overall health and immunity. The two primary lymphoid organs of prime importance are the red bone marrow and the thymus.
The red bone marrow is a soft, spongy tissue nestled in the interior of long bones such as the humerus and femur. It is the site...
Cells of the Adaptive Immune Response01:23

Cells of the Adaptive Immune Response

The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...
Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

Overview

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Wild-type Blocking PCR Combined with Sanger Sequencing for Detection of Low-frequency Somatic Mutation
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Therapy-associated lymphoid proliferations.

Adam Bagg1

  • 1Department of Pathology & Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104-4283, USA. adambagg@mail.med.upenn.edu

Advances in Anatomic Pathology
|April 15, 2011
PubMed
Summary
This summary is machine-generated.

Therapy-related lymphoid proliferations can arise after transplantation or from treatments for other conditions. These conditions, including therapy-related acute lymphoblastic leukemia and autoimmune diseases, have diverse causes and outcomes.

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Area of Science:

  • Oncology
  • Immunology
  • Hematology

Background:

  • Therapy-related lymphoid proliferations are recognized post-transplantation under immunosuppression.
  • Recent observations indicate these proliferations also occur in patients treated for other conditions.
  • These diverse conditions share a common link to medical therapies.

Purpose of the Study:

  • To review two distinct scenarios of therapy-related lymphoid proliferations.
  • To explore the divergent pathogeneses and consequences of these conditions.
  • To differentiate mechanisms in therapy-related acute lymphoblastic leukemia versus those in autoimmune disease settings.

Main Methods:

  • Literature review focusing on therapy-related lymphoid proliferations.
  • Analysis of cases associated with chemotherapy (topoisomerase II inhibitors) for neoplasms.
  • Examination of cases arising in the context of autoimmune diseases and their treatments.

Main Results:

  • Therapy-related acute lymphoblastic leukemia often results from direct DNA damage due to chemotherapy.
  • Lymphoid proliferations in autoimmune diseases are heterogeneous, complex, and not always overtly neoplastic.
  • Pathogenesis varies based on the underlying autoimmune disease and therapeutic interventions.

Conclusions:

  • Therapy-related lymphoid proliferations encompass diverse entities with distinct origins.
  • Chemotherapy-induced DNA damage is a key factor in therapy-related acute lymphoblastic leukemia.
  • Autoimmune disease-associated proliferations present complex pathogenetic mechanisms influenced by disease and treatment variability.