1. Copyright © 1999 American Medical Association. All rights reserved.
From: Impairment of T-Cell Activation in Head and Neck Cancer In Situ and In VitroStrategies for an Immune Restoration
Arch Otolaryngol Head Neck Surg. 1999;125(1): doi: /archotol
Figure Legend:
Immunostaining of squamous cell carcinoma of the head and neck biopsy specimens. A, Carcinoma cells show high levels of intercellular adhesion molecule-1 (ICAM-1) expression (anti–ICAM-1 avidin-biotin peroxidase complex [ABC-PO], original magnification ×400). B, Similar staining pattern for lymphocyte function associated antigen-3 (LFA-3), with intensive staining of both the inflammatory cells and carcinoma cells (arrow) (anti–LFA-3 ABC-PO, original magnification ×200). C and D, Absence of B7.1 (CD80; part C) and B7.2 (CD86; part D) on carcinoma cells (arrow). In contrast, lymphocytes and antigen-presenting cells (APC) exhibit strong positivity for both antigens (anti–B7.1 ABC-PO and anti-B7.2 alkaline anti-alkaline phosphatase [APAAP], original magnification ×400). E, Double staining allows discrimination between B7.2-negative carcinoma cells as detected by pancytokeratin antibody KL1 (red) and CD86 (B7.2)–positive lymphocytes and APC (brown; arrow) (anti–B7.2 ABC-PO and anti–pancytokeratin APAAP, original magnification ×400). F, Expression of CD40 on APC and on carcinoma cells. The endothelium of blood capillaries, used as an "internal standard" also exhibited a well-delineated and strong positivity (arrow) (anti–CD40 ABC-PO, original magnification ×200). G and H, Expression of class I major histocompatibility complex (MHC) on the surface of carcinoma cells (arrow) and inflammatory cells (part G); class II MHC molecules are only detectable on APC but not on tumor clusters (arrow) (part H) (anti–class I MHC and class II MHC ABC-PO, original magnification ×200).
Date of download: 10/24/2017
Copyright © 1999 American Medical Association. All rights reserved.

2. Copyright © 1999 American Medical Association. All rights reserved.
From: Impairment of T-Cell Activation in Head and Neck Cancer In Situ and In VitroStrategies for an Immune Restoration
Arch Otolaryngol Head Neck Surg. 1999;125(1): doi: /archotol
Figure Legend:
Expression of adhesion, costimulatory, or major histocompatibility complex (MHC) molecules on human squamous carcinoma cell line PCI-1, as detected by flow cytometry. The cell line PCI-1 was stained either with the fluoroscein isothiocyanate (FITC)–labeled monoclonal antibodies of interest (black line) or with the FITC-labeled isotype-matched control monoclonal antibody (gray line). A total of 5000 cells were analyzed for each sample. A, intercellular adhesion molecule-1 (CD54); B, lymphocyte function associated antigen-3 (CD58); C and D, absence of B7.1 (CD80; C) or B7.2 (CD86; D); E, CD40; F, class I MHC; and G, absence of class II MHC (HLA-DR).
Date of download: 10/24/2017
Copyright © 1999 American Medical Association. All rights reserved.

3. Copyright © 1999 American Medical Association. All rights reserved.
From: Impairment of T-Cell Activation in Head and Neck Cancer In Situ and In VitroStrategies for an Immune Restoration
Arch Otolaryngol Head Neck Surg. 1999;125(1): doi: /archotol
Figure Legend:
Proliferation of peripheral blood T lymphocytes (PBL-T) stimulated by irradiated squamous cell carcinoma of the head and neck cells in the presence of 1-µg/mL phytohemagglutinin-P. Note the significant inhibition of proliferation (P<.001) in cocultures with parental (Par) or LacZ-transduced PCI-13, and the complete restoration significantly (P<.001) exceeding the baseline value in the presence of B7.1 (bars indicate means ± SDs of sixplicate wells). A representative experiment of 3 performed.
Date of download: 10/24/2017
Copyright © 1999 American Medical Association. All rights reserved.

4. Copyright © 1999 American Medical Association. All rights reserved.
From: Impairment of T-Cell Activation in Head and Neck Cancer In Situ and In VitroStrategies for an Immune Restoration
Arch Otolaryngol Head Neck Surg. 1999;125(1): doi: /archotol
Figure Legend:
Model of the distinct stages of the antigen-specific activation of T cells by antigen-presenting cells (APC) in the tumor microenvironment. First, adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function associated antigen-3 (LFA-3) mediate the binding between APC and T lymphocytes (1). T cells recognize antigenic peptides presented by major histocompatibility (MHC) molecules (2) on APC, resulting in up-regulation of the CD40 ligand on T cells and induction of B7 molecules on APC (3). This costimulatory stimulus, ie, triggering of CD40 on APC and CD28 on T cells, prevents clonal anergy and leads to the generation of an efficient T-cell response. Regarding the preserved expression of ICAM-1 and LFA-3 necessary for adhesion, the transduction of the B7.1 gene into tumor cells can bypass the "missing link," ie, the absence of class II MHC, CD80 or CD86, respectively, thus forcing these cells to function as APC. AG indicates antigen; TCR, T-cell receptor; IL-2, interleukin 2; GM-CSF, granulocyte-macrophage colony-stimulating factor; and TNF, tumor necrosis factor.
Date of download: 10/24/2017
Copyright © 1999 American Medical Association. All rights reserved.