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CD7

Official Full Name
CD7 molecule
Organism
Homo sapiens
GeneID
924
Background
This gene encodes a transmembrane protein which is a member of the immunoglobulin superfamily. This protein is found on thymocytes and mature T cells. It plays an essential role in T-cell interactions and also in T-cell/B-cell interaction during early lymphoid development. [provided by RefSeq, Jul 2008]
Synonyms
GP40; TP41; Tp40; LEU-9;
Protein Sequence
MAGPPRLLLLPLLLALARGLPGALAAQEVQQSPHCTTVPVGASVNITCSTSGGLRGIYLRQLGPQPQDIIYYEDGVVPTTDRRFRGRIDFSGSQDNLTITMHRLQLSDTGTYTCQAITEVNVYGSGTLVLVTEEQSQGWHRCSDAPPRASALPAPPTGSALPDPQTASALPDPPAASALPAALAVISFLLGLGLGVACVLARTQIKKLCSWRDKNSAACVVYEDMSHSRCNTLSSPNQYQ
Open
Disease
Leukaemia, Lymphoma, Malignant haematopoietic neoplasm, Mycosis fungoides
Approved Drug
0
Clinical Trial Drug
2 +
Discontinued Drug
0

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Detailed Information

Crucially important in the immune system, the CD7 gene codes for a transmembrane protein of the immunoglobulin superfamily. Found mostly on thymocytes and mature T cells, this 40 kDa single-chain glycoprotein, 240 amino acid residue, is essential for T-cell contacts and T-cell/B-cell communication during early lymphoid development. Although CD7 is a necessary molecule, its expression is not homogeneous; some normal T lymphocytes lack CD7, which does not affect their formation, maturation, or general activity.

Found on chromosome 17, the CD7 gene produces mRNA via a transcriptional mechanism producing four exons across around 3.0 kb. Among the many portions of the CD7 molecule these exons encode are an immunoglobulin-like domain, a fusion domain, a transmembrane domain, and a cytoplasmic domain. Every one of these parts helps to explain the many ways in which CD7 controls T-cell development and differentiation at various phases of life.

Significantly, CD7 has attracted a lot of attention in the field of cancer treatment—especially in CAR-T cell therapy. CD7 rapidly internalizes when it interacts with antibodies or antibody-derived compounds, therefore providing a difficult environment for therapeutic approaches aiming at CD7. As they also unintentionally target and kill CD7-positive CAR-T cells themselves, this presents a conundrum in CAR-T cell treatments meant to eradicate CD7-expressing tumor cells. During the in vitro growth phase, this phenomenon causes a significant drop in the CAR-T cell count. Researchers are looking at techniques to reduce CD7 expression in CAR-T cells to improve their effectiveness and lifespan, therefore addressing this problem.

Figure 1 illustrates the signaling pathways activated by the T cell receptor and the additional role of signals generated by CD7 in T cell signal transduction.Figure 1. A schematic representation of T cell signal transduction pathways initiated by the TCR, illustrating the contributions of signals generated by CD7.

CD7-Mediated Signaling Pathways

Several signaling pathways influencing immune cell activation and differentiation depend on the CD7 molecule. Among its important functions are T-cell activation and differentiation. Engagement with different ligands allows CD7 to cause significant cellular reactions. For instance, ligands like concanavalin A cause thymocytes' and mature T cells' death. On lymphocytes, endogenous lectins interact with early-expression CD7 molecules to help cellular selection using the Ga11-mediated signaling pathway. Gal1 is another crucial ligand that helps T cells in peripheral blood mononucleated cells (PBMCs) be activated and proliferated. It induces T cells to release important cytokines including IL-2, TNF-alpha, TNF-beta, and GM-CSF as well as express interleukin-2 receptor (I-2Ra).

Furthermore, the fast influx of calcium ions across the cell membrane resulting from the interaction of CD7 with other molecules including CD3 sets off T-cell activation. Important interactions between CD7 and the T-cell receptor (TCR) also support integrin-mediated adhesion between T cells and other ligands including fibronectin, ICAM-1, and VCAM-1. In response to signaling molecules, CD7 similarly mediates the transmembrane flow of calcium ions, therefore promoting NK cell activation and hence improving NK cell cytotoxicity and adhesion characteristics.

Potential Applications of Targeting CD7

Given its major expression in many hematological malignancies, CD7 is a fundamental tumor cell surface marker. Among lymphoblastic leukemia and lymphomas as well as a subgroup of peripheral T-cell lymphomas, over 95% express CD7. Targeting CD7 does not negatively affect the functional capability of peripheral blood T cells, so it is a desirable target for therapeutic approaches including anti-CD7 antibody-drug conjugates (ADCs).

T-cell Acute Lymphoblastic Leukemia (T-ALL)

With 15% in children and about 25% of adult acute lymphoblastic leukemia (ALL) cases represented by T-ALL, this extremely aggressive type of hematological malignancy accounts for About 64,000 fresh ALL cases reported worldwide every year. Usually including chemotherapy and stem cell transplantation, the usual treatment approach has an overall response rate of about 30%–40%. The median general survival for responding patients is around six months, which emphasizes how urgently additional successful treatment strategies are needed. Targeting this cancer successfully with CD7-CAR-T treatments makes sense given the elevated expression of CD7 in T-ALL.

Acute Myeloid Leukemia (AML)

With about 70% of patients experiencing symptom alleviation but then relapsing into refractory illness, which usually leads to treatment failure and death, AML is the most prevalent acute leukemia among adults and treatment mostly depends on chemotherapy. Frequently linked with abnormal bone marrow hyperplasia, reduced MPO expression, and increased CD7 expression levels, the CD7 molecule has been shown as a negative prognostic marker in AML.

NK/T-cell Lymphoma (NKTL)

Rapid disease advancement defines the diverse and aggressive hematological malignancy that NKTL, a subtype of non-Hodgkin lymphoma (NHL), exhibits. Early T-cell lineage markers include CD2, CD3, CD5, and CD7 rather than particular antigens, early NK cells and T cells in NKTL show an overexpression. This draws attention to how one may target CD7 to cure NKTL.

Solutions in CD7-CAR-T Development

The development of CD7-CAR-T treatments poses numerous difficulties. CD7 is first a pan-T-cell antigen, so most T cells express it. This broad expression may cause notable self-targeting, which lowers the supply of functional CAR-T cells fit for use in therapy. Second, technically difficult and expensive is still the procedure of separating and growing enough normal autologous T cells from patient blood or bone marrow. Moreover, using CAR-T cells produced from healthy donor T cells might generate questions about severe graft-versus-host disease (GVHD) in patients.

Researchers are looking at ways to solve these problems using methods to eradicate CD7 expression in CAR-T cells themselves. One strategy entails completely deleting the CD7 gene; another uses a technique wherein the CD7-binding domain is fixed within the endoplasmic reticulum, therefore preventing the CD7 protein from reaching the cell surface. These modified CAR-T cells, devoid of CD7, retain their proliferative capacity and cytotoxic properties mediated by the CAR, hence reducing self-targeting events. Moreover, these CD7-negative CAR-T cells show strong cytotoxic action against CD7-positive hematological cancers, hence improving their therapeutic possibilities.

ADCs aiming at CD7 have also entered clinical testing outside of CAR-T and CAR-NK forms. One such contender, T-Guard, uses a dual ADC strategy combining anti-CD7 with RTA with anti-CD3. Currently in phase III studies, this marks the height of research on CD7-targeted treatments; yet safety issues have caused this temporary suspension from clinical review.

References:

  1. Dai Z, Mu W, Zhao Y, et al. T cells expressing CD5/CD7 bispecific chimeric antigen receptors with fully human heavy-chain-only domains mitigate tumor antigen escape. Signal Transduct Target Ther. 2022;7(1):85. Published 2022 Mar 25.
  2. Soare DS, Radu E, Dumitru I, et al. FLT3-ITD DNA and mRNA levels in AML do not correlate with CD7, CD33, and CD123 expression. J Cell Mol Med. 2020;24(13):7675-7679.
  3. Lv K, Cai C, Chen J, et al. Prognostic value of lymphoid marker CD7 expression in acute myeloid leukemia patients undergoing allogeneic hematopoietic cell transplantation in first morphological complete remission. Int J Hematol. 2021;114(4):464-471.
  4. Stillwell R, Bierer BE. T cell signal transduction and the role of CD7 in costimulation. Immunol Res. 2001;24(1):31-52.
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